BIMONTHLY ASSIGNMENT - MAY 2021

 

Note: I have been assigned the following cases to solve the related questions in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations, diagnosis and the treatment regimen.

Note: The information in this assignment has also been obtained from various sources that I have referenced and acknowledged with their online links and I have paraphrased them further. However the images I have borrowed may have copyright issues as they may not be certified through a creative commons license in which case, I hope the original authors will get in touch with me and I shall remove them if they wish.

CARDIOLOGY

Case 1

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 1

1.What is the difference between heart failure with preserved ejection fraction and with reduced ejection fraction?

Ans. In heart failure with reduced ejection fraction (HFrEF), the left side of your heart is weak and can’t pump enough blood to the rest of your body. Chronic (long-term) conditions that damage or weaken the heart muscle are the main cause of heart failure with reduced ejection fraction. For example, coronary heart disease or a heart attack can prevent your heart muscle from getting enough oxygen. Other causes of this type of heart failure include faulty heart valves, an irregular heartbeat, or heart diseases that you are born with or inherit.

How a heart attack can lead to heart failure. Above figure A shows dead heart muscle caused by a heart attack. Figure B is a close-up showing how a blocked artery in the heart prevents the heart muscle from getting oxygen. The heart muscle begins to die, weakening the heart.

• In heart failure with preserved ejection fraction (HFpEF), the left side of your heart is too stiff to fully relax between heartbeats. That means it can't fill up with enough blood to pump out to your body. High blood pressure and other conditions that make your heart work harder are the main causes of heart failure with preserved ejection fraction. Conditions that stiffen the chambers of the heart such as obesity and diabetes are also causes of this type of heart failure. Over time, your heart muscle thickens to adapt, which makes it stiffer. 

Note: This patient is diabetic and hypertensive. 

Diagnosis: An echocardiography measures the patient's ejection fraction. Your ejection fraction is the percent of the blood in the lower left chamber of your heart (the left ventricle) that is pumped out of your heart with each heartbeat. Ejection fraction indicates how well your heart pumps. This helps to diagnose the type of heart failure and guide treatment. 

• If 40% or less of the blood in the left ventricle is pumped out in one beat, it is heart failure with reduced ejection fraction. 
• If 50% or more of the blood in the left ventricle is pumped out in one beat, it is heart failure with preserved ejection fraction. 
• If ejection fraction is somewhere in between (41% to 49%), maybe diagnosed with heart failure with borderline ejection fraction. 

Note: This patient had ejection fraction of 58%

REFERENCES:

1. https://www.nhlbi.nih.gov/health-topics/heart-failure

2.Why haven't we done pericardiocentesis in this patient?        

Ans. Pericardiocentesis was not done in this patient due to following:

• In case of pericardial effusion in this patient which was 20.7 mm at admission and resolved to 14mm by discharge date. 

  Pericardiocentesis for diagnostic purposes is not justified in cases of mild or moderate effusions (<20 mm) for the following reasons

1) Low diagnostic power (the underlying pathology is often already known or identifiable through different non-invasive tests).

2) Viral (idiopathic) pericarditis is usually self-limiting and only requires an anti-inflammatory treatment.

3) High procedural risk compared with low diagnostic yield.

• Without hemodynamic compromise, pericardiocentesis is indicated for:

- symptomatic moderate to large effusion non-responsive to medical therapy OR in case of a smaller effusion when tuberculous, bacterial or neoplastic pericarditis is suspected OR in case of chronic (lasting more than three months) OR large pericardial effusion (>20 mm on echocardiography in diastole).
None of the above criteria were met by our patient as confirmed by investigations.

• 2004 ESC guidelines1 support the use of pericardiocentesis if purulent, tuberculous, or neoplastic pericarditis is suspected. Pericardiocentesis can also be performed for patients with persistent symptomatic pericardial effusions.

• Pericardiocentesis is also the management for cardiac tamponade which was not detected in this patient.

• Post-infarction rupture of the free wall is a contraindication to needle pericardiocentesis due to the potential risk of aggravating the myocardial rupture via rapid pericardial decompression and restoration of systemic arterial pressure - due to potential past MI ?

REFERENCES:

1. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Pericardiocentesis-in-cardiac-tamponade-indications-and-practical-aspects
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878263/

3. What are the risk factors for development of heart failure in the patient?

Ans. Heart failure is a condition that develops when your heart doesn’t pump enough blood for your body’s needs. The following could be the risk factors in this patient:

1. Age - Patient is 78 years. People 65 years or older have a higher risk of heart failure because aging can weaken and stiffen your heart.
2. Lifestyle habits - Patient is a chronic smoker + alcoholic, which increases his risk of heart failure.
3. Comorbidities - Patient is a K/C/O Diabetes Mellitus and Hypertension. 
4. Previous MI? Pericardial and pleural effusion? - leading to pericarditis?

REFERENCES:

• https://www.nhlbi.nih.gov/health-topics/heart-failure

4. What could be the cause for hypotension in this patient?

Ans. - It could be drug induced. 

Since the patient takes Telmisartan for HTN and is a diabetic/chronic alcoholic/ impaired creatinine levels and is >70 years, it could lead to hypotension.

         - It could be due to viral infection? viral myocarditis?

Case 2

https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html. 

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 2

1.What could be the possible causes of heart failure in this patient?

Ans. The patient has the following risk factors/symptoms discovered on history taking, examination and investigation which could be the cause for heart failure:

1. Obesity - Central Truncal
2. Diabetes Mellitus
3. Chronic Kidney Disease - Stage 4 in this patient.
4. Hypertension
5. Atrial Fibrillation
6. Anemia - HB was 7.5gm/dl with normochromic normocytic anemia
7. Chronic smoking and alcohol intake.
8. Age - 73 years.

The above causes could gradually change the structure and function of the heart over time, with changes that stiffen the heart, making it more difficult for it to fill appropriately leading to symptoms of HFpEF resulting from the accumulation of blood/fluid in the lungs, veins and tissues of the body. 

• Fluid backs up into these areas because the heart is not filling adequately. The buildup of fluid in the lungs can result in shortness of breath while fluid in the legs caused swelling/pedal edema in this patient.

REFERENCES:

1. https://www.umcvc.org/conditions-treatments/heart-failure-preserved-ejection-fraction-hfpef
2. https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.119.313572

2. What is the reason for anemia in this case?

Ans. This patient was diagnosed with CKD - stage 4 and Diabetes Mellitus -Type 2.

1. Causes of anemia in CKD may include:

• Inflammation
• Low levels of EPO (erythropoietin) due to kidney damage as kidney is the main source of EPO.
• Low levels of the nutrients needed to make red blood cells.
• Shortened red blood cell survival.

 

      

    2. Causes of anemia in DM may include:

• The elevation of proinflammatory cytokines plays an essential role in insulin resistance and induces the appearance of cardiovascular complications diabetic micro- and macrovascular, kidney disease and anemia.
• By increasing especially IL-6, anti-erythropoietic effect occurs, since this cytokine changes the sensitivity of progenitors to erythropoietin (erythroid growth factor) and also promotes apoptosis of immature erythrocytes causing a decrease, further, in the number of circulating erythrocytes and consequently causing a reduction of circulating hemoglobin

NOTE: According to Escorcio et al. approximately 40% of diabetic patients are affected by kidney diseases. The decreased renal function and proinflammatory cytokines are the most important factors in determining reduction of hemoglobin levels in those patients. 

The inflammatory situation created by kidney disease also interferes with intestinal iron absorption and mobilization of inventories. 

Therefore, diabetic patients with kidney disease have the highest risk for developing anemia- Anemia of Chronic Disease.

 REFERENCES: 

1. https://www.niddk.nih.gov/health-information/blood-diseases/anemia-inflammation-chronic-disease
2. https://jasn.asnjournals.org/content/23/10/1631
3. https://www.hindawi.com/journals/anemia/2015/354737/

3. What is the reason for blebs and non healing ulcer in the legs of this patient?

Ans.  Spontaneous blebs/bullae may be the first sign of underlying impaired glycemic control, with associated nephropathy and neuropathy - this patient has Diabetic Triopathy.

• Leading to the hypothesis of an underlying associated local sub-basement membrane-zone connective-tissue alteration and micro-angiopathy causing blisters/blebs. 
• These are a spontaneous, distinct, non-inflammatory, blistering condition of the skin predominantly seen in patients with diabetes mellitus. 
• Lesions have a predilection for the distal lower extremities more than the upper extremities, especially the tips of the toes and plantar surfaces of the feet - as in this patent on the 3rd toe of left foot.

 Evidence suggests that poor mobility and cognitive and visual impairment are major risk factors for RTA and Traumatic Non- Healing injuries in individuals with Diabetes, chronic alcoholics.

• Wound healing occurs as a cellular response to injury and involves activation of keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets. Many growth factors and cytokines released by these cell types are needed to coordinate and maintain healing.
• Risk factors are primarily related to hypoglycemic conditions associated with antidiabetic therapy, which include:

1. Decreased or impaired growth factor production.
2. Angiogenic response.
3. Macrophage function. 
4. Collagen accumulation. 
5. Epidermal barrier function. 
6. Quantity of granulation tissue.
7. Keratinocyte and fibroblast migration and proliferation.
8. Number of epidermal nerves.
9. Bone healing.
10. Balance between the accumulation of ECM components and their remodeling by MMP

Risk factors in this patient which could have attributed to non-healing leg ulcer:

Local Factors	Systemic Factors
Oxygenation Infection Foreign body Venous sufficiency	Age and gender Sex hormones Diseases: Diabetes Type 2, Chronic Kidney Disease, Hypertension Obesity - Central Truncal Alcoholism - Chronic Intake Medications used?? any steroids or NSAIDS?? Immunocompromised condition, Previously COVID positive?? Nutrition, Anemia

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1857239/
2. https://bjdabcd.com/index.php/bjd/article/view/52/120#:~:text=Diabetic%20bullae%2C%20also%20known%20as,reported%20in%201930%20by%20Kramer.
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903966/

4. What sequence of stages of diabetes has been noted in this patient?

Ans. Introduction: Two leading US diabetes groups have issued a joint position statement revealing the four stages of type 2 diabetes. The model emphasizes the importance of type 2 diabetes prevention during the first phase, when signs of insulin resistance begin to emerge.

The American Association of Clinical Endocrinologists (AACE) and the American College of Endocrinology (ACE) combed through clinical evidence and research to come up with the four phases.

1. Insulin Resistance

2. Prediabetes

3. Type 2 Diabetes Mellitus

4. Type 2 Diabetes + Vascular complications

- Retinopathy, Nephropathy or Neuropathy, related Microvascular events.

Sequence of stages in this patient:

1. Prediabetes

- asymptomatic before 30 years, chronic alcohol intake.

 🠗

2. Type 2 DM

- Symptomatic and diagnosed 30 years back, treated since then.

- Obese, Age 43 years, Chronic Alcohol intake

 🠗

3. Diabetic Nephropathy

- Since 4 years

- SOB, Pedal edema, CDK stage 4, Increased Creatinine levels.

 🠗

4. Diabetic Retinopathy

- Since 4 years

- Blurring of vision

 🠗

5. Vascular - Non healing ulcer

- 10 days back

- RTA traumatic injury 

REFERENCES:

1. https://www.diabetes.co.uk/news/2018/dec/four-stages-of-type-2-diabetes-identified-by-us-doctors99311412.html#:~:text=The%20statement's%20four%20stages%20of,%2C%20or%2C%20related%20microvascular%20events.

Case 3

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 3

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans. The evolution of the symptomatology is as follows: 

10 Years ago - Inguinal Hernia Surgery

- On/off pain at surgical site

⬇️

Since 3 Years - Aggravated pain at surgical site

⬇️

Since 2 to 3 Years - On/Off facial puffiness

⬇️

Since 1 Year - Hypertension

⬇️

Since 1 Year -  SOB grade 2

- when hospitalized, HTN diagnosed.

⬇️

2 Days ago - SOB grade 2 progressed to grade 4

⬇️

Since 2 Days - Decreased Urine Output and Constipation

⬇️

Since Morning - Anuria

Patient has h/o NSAID abuse since 3 years.

Anatomical location:

Based on the CT picture, the site of abnormality is the Atrial septum - ASD.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Hypertension

2. Renal dysfunction - Increased creatinine, hypoalbuminemia

3. NSAID abuse. 

REFERENCES:

• https://www.nhs.uk/conditions/atrialfibrillation/causes/#:~:text=The%20exact%20cause%20of%20atrial,atherosclerosis

2. What are mechanism of actions, indications and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans. The following interventions were used in this patient: 

1. Inj. Dobutamine 3.6ml/hr

• β1-agonist
• Indicated for the Congestive cardiac failure that the patient presented with.
• Sustained improvement of cardiac function in patients with congestive heart failure after short-term infusion of dobutamine.
• Reference: https://pubmed.ncbi.nlm.nih.gov/6357536/

 2. Tab. Digoxin 0.25mg OD

• Digitalis glycosides
• Indicated for the Congestive cardiac failure that the patient presented with.
• The goal of digoxin therapy in patients with congestive heart failure is to improve quality of life by reducing symptoms and preventing hospitalizations.

• Reference: https://www.aafp.org/afp/2000/0715/p409.html

3. Inj. Unfractionated Heparin 5000 IU TID.

• Anticoagulant
• Reduces the risk of thrombi formation and embolization in atrial fibrillation. 

• Reference : https://www.ahajournals.org/doi/full/10.1161/hq0701.093686

4. Tab. Carvedilol 3.125mg BD

• Vasodilatory Non-selective Beta Blocker
• Indicated for Atrial fibrillation, hypertension, heart failure.
• Escalating doses of oral carvedilol can be effectively and safely used in the acute treatment of AF with fast ventricular rate.

• Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231552/ 

5. Tab. Acetyl cysteine 600mg PO TID.

• Mucolytic, for NSAID abuse??
• Also it is a free radical scavenger which could reduce the oxidative stress in atrial fibrillation?

• Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331849/#:~:text=An%20increasing%20body%20of%20evidence,of%20postoperative%20AF%20(POAF).

6. Daily monitoring of APTT, PT, INR and RFT was done. 

• The therapeutic effect of oral anticoagulants (OACs) is measured by monitoring the prothrombin time.
• OAC dosage must be adjusted to achieve a narrow range of the desired prothrombin time values, usually expressed as the international normalized ratio (INR).Thromboplastins, the essential reagent for prothrombin time testing.

7. Tab. Acitrom 2mg OD 

• Oral Anticoagulant
• Indicated in Atrial Fibrillation
• prevention of the intrahepatic metabolism of vitamin K epoxides, and an induction of vitamin K deficiency. As a result, thrombin generation slows, and clot formation becomes impaired due to decreased biologic activity of the prothrombin complex proteins.
• Significant stroke reduction in primary and secondary prevention and Significant reduction in total mortality compared to placebo.

• Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768341/

3. What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

Ans. Heart performance and kidney function are closely interconnected physiologically and patho-physiologically. 

• Risk factors include:  hypertension, diabetes, elderly age, and prior history of heart or renal failure. NSAID Abuse could have caused Renal dysfunction in this patient.
• The pathophysiology of the cardiorenal syndrome involves intrarenal hemodynamics, trans-renal perfusion pressure and systemic neurohormonal factors, compromise of the net renal perfusion pressure, inadequate cardiac output and decreased perfusion pressure. 
• In the presence of risk factors such as hypertension as this patient, there is further reduction of glomerular filtration.
• Neurohumoral activation mediated by activation of arterial baroreceptors and intrarenal sensors. These reflexes lead to the activation of the renin-angiotensin system, sympathoadrenal system and arginine-vasopressin system – an intrinsic self-defense system to maintain blood pressure and intravascular volume. 
• All of these factors will lead to peripheral and intrarenal vasoconstriction, further decreasing renal blood flow and GFR, and leading to a decrease in renal function. 
• The consequences also lead to renal hypoxia, inflammation, cytokine release, and progressive structural and functional loss. 
• The net clinical consequences are sodium and fluid retention, increased urea, uric acid and creatinine levels and progressive reduction of renal function.

Clinical correlation between kidney and heart disease. This is a summary of close relationship between renal failure main features and equivalent heart involvement with particular focus on uremia effects on systolic and diastolic left ventricular function.

The patient has Cardiorenal syndrome type 4
Due to the involvement of Cardiovascular System with primary renal disease, with Ventricular hypertrophy and diastolic dysfunction. 





Pathophysiological pathways of type-4 cardiorenal syndrome. It has been highlighted the role of uremia in developing minor and major cardiovascular complications referring to main CKD-related cardiovascular risk factors such as secondary hyperparathyroidism, anemia, accelerated atherosclerosis and chronic inflammation.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2794438/
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5415026/

4. What are the risk factors for atherosclerosis in this patient?

Ans. Risk factors in this patient would include:

1. Hypertension
2. Old age
3. Male gender
4. NSAID abuse? leading to renal disease

5. Why was the patient asked to get those APTT, INR tests for review?

Ans. In an effort to standardize the monitoring of Oral anticoagulants, the INR was adopted worldwide. The INR converts the prothrombin (PT) patient/PT mean normal ratio to the value expected if the test had been performed with the WHO reference thromboplastin.

International normalized ratio (INR)

1. It is the preferred test of choice for patients taking vitamin K antagonists (VKA).
2. It can also be used to assess the risk of bleeding or the coagulation status of the patients. 
3. Patients taking oral anticoagulants are required to monitor INR to adjust the VKA doses.
4. The INR is derived from prothrombin time (PT) which is calculated as a ratio of the patient’s PT to a control PT standardized for the potency of the thromboplastin reagent developed by the World Health Organization (WHO) using the following formula:

• INR = Patient PT ÷ Control PT

The Activated Partial Thromboplastin Time (APTT)

1. It is the most commonly used test for laboratory monitoring of unfractionated heparin therapy
2. Laboratory monitoring is widely recommended to measure the anticoagulant effect of unfractionated heparin and to adjust the dose to maintain levels in the target therapeutic range. 
3. The focus of clinicians who manage unfractionated heparin therapy should be to ensure that an adequate starting dose of unfractionated heparin is used and that the aPTT method is standardized.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768341/
2. https://www.ncbi.nlm.nih.gov/books/NBK507707/
3. https://pubmed.ncbi.nlm.nih.gov/8725715/
4. https://pubmed.ncbi.nlm.nih.gov/17080209/#:~:text=Laboratory%20monitoring%20is%20widely%20recommended,partial%20thromboplastin%20time%20(aPTT)

Case 4

https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 4

1. How did the patient get relieved from his shortness of breath after IV fluids administration by rural medical practitioner?

Ans. The patient was in hypovolemic shock which had triggered the SOB, on administering IV fluids, hypovolemia was corrected and SOB was relieved.

2. What is the rationale of using Torsemide in this patient?

Ans. The ACCF/AHA has given a Class I recommendation for the use of diuretics (including loop diuretics) as the first-line treatment of heart failure with reduced left ventricular ejection fraction (HFrEF) and volume overload.

• MOA- Loop diuretics such as Torsemide induce its effect by competing with chloride to bind to the Na-K-2Cl (NKCC2) cotransporter at the apical membrane of the thick ascending limb of the loop of Henle and blocking the cotransporter, which inhibits the reabsorption of sodium and chloride. By inhibiting NaCl reabsorption, tonicity in the interstitium decreases, and free water excretion increases as a result.
• Advantages of Torsemide over other loop diuretics:

1. Torsemide is known to have the longest half-life at 3 to 4 hours and can be as long as 5 to 6 hours in patients with renal/hepatic dysfunction or heart failure.
2. Torsemide provides the longest duration of action and can give even greater diuretic effects in patients that have hepatic dysfunction or heart failure.

REFERENCES:

• https://www.ncbi.nlm.nih.gov/books/NBK546656/

3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

Ans. Due to presence of whitish discharge and pus cells in urine on examination, Ceftriaxone was administered to this patient as UTI is a possibility due to maybe Gonorrhea bacteria.

Case 5

https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

 Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 5

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans. The evolution of the symptomatology is as follows: 

3 Days ago - Mild Chest pain

- Right side, radiating to back (retrosternal)

- Insidious onset, Gradual progression

⬇️

3Days ago - Giddiness

- Not increasing/decreasing with change of position

⬇️

Since 3 Days - Profuse sweating

⬇️

Since 3 Days - Disturbed sleep due to discomfort

Patient is a K/C/O Diabetes Mellitus Type 2 Since 8 years and Hypertension.

Anatomical location:

As the patient suffered from Inferior wall myocardial infarction (MI) which occurs from a coronary artery occlusion with resultant decreased perfusion, ischemia and infarction to that region of the myocardium, the localization of the problem lies in the - inferior myocardium supplied by the right coronary artery.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Hypertension - high blood pressure 

2. Type 2 DM - uncontrolled blood sugars 

3. Age 

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/books/NBK470572/

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans. 

• Tab. ASPIRIN 325 mg PO/STAT

1. Salicylate, NSAID
2. Indicated to reduce the blood clot formation in coronary artery in Inferior wall MI in this patient.
3. Aspirin used for secondary prevention of atherothrombotic events.

Reference: https://www.ahajournals.org/doi/full/10.1161/circulationaha.116.023952

• Tab ATORVAS 80mg PO/STAT

1. Statin, HMG Co-A reductase inhibitor, decreased cholesterol production.
2. Indicated to reduce FFA's, has anti-inflammatory and antithrombotic effects too in MI.
3. Free fatty acid levels showed a sharp increase during the acute phase of MI. Treatment with atorvastatin 20 mg/day, and especially with 40 mg/day, resulted in a decrease in free fatty acid levels. The positive effect of low-dose atorvastatin (20 mg/day) is normalization of the adipokine status. Administration of atorvastatin 20 mg/day was accompanied with a statistically significant reduction in glucose levels (by 14%) and C-peptide levels (by 38%), and a decrease in the homeostasis model assessment of insulin resistance index on day 12.

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4492625/#:~:text=Results,normalization%20of%20the%20adipokine%20status.

• Tab CLOPITAB 300mg PO/STAT

1. Antiplatelet drug, blood thinner
2. Addition of Clopidogrel to aspirin reduces the risk of major ischemic events by up to a further one-third in patients with STEMI treated with fibrinolytic therapy and undergoing percutaneous coronary intervention, with no significant increase in bleeding. Thus, dual antiplatelet therapy with the combination of clopidogrel and aspirin is becoming the new standard of care for the management of patients with STEMI.

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994022/

• Inj HAI 6U/IV STAT

1. Human Actrapid Insulin used to reduce high blood sugar levels in diabetes patients.
2. Fast acting, Insulin infusion improves myocardial blood flow in the ischemic and non-ischemic regions in subjects with type 2 diabetes.

Reference: https://diabetes.diabetesjournals.org/content/55/2/511

• Angioplasty with stent placement

1. Angioplasty is a procedure to open narrowed or blocked coronary arteries that supply blood to the heart.  
2. A coronary artery stent is a small, metal mesh tube that expands inside a coronary artery. A stent is often placed during or immediately after angioplasty.
3. Coronary intervention techniques like angioplasty and stent placement reproduce reperfusion in a significant number of patients.

Reference: https://pmj.bmj.com/content/75/888/591

3. Did the secondary PTCA do any good to the patient or was it unnecessary?

Ans. The secondary PTCA seems to be unnecessary as the thrombolytic therapy reduced the symptoms and patient was doing better and the procedure was done after the window period of 12 hours.

1. The concomitant use of primary angioplasty and thrombolysis (facilitated angioplasty) is considered experimental and has no place in routine management of acute MI at this time.
2. Best outcomes occur when primary PCI is performed with a door-to-balloon time of < 90 minutes and when symptoms onset was < 12 hours. Primary PCI is only indicated when symptoms duration is 12-24 hours (delayed presentation) if severe congestive heart failure, hemodynamic/electrical instability or continued angina is present. Primary PCI is not recommended when symptom onset is more than 12 hours and the patient is asymptomatic (OAT trial).

 

REFERENCE:

• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387753/
• https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/coronary-artery-disease-stemi/treatment-revascularization

Case 6

https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 6

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans. The evolution of the symptomatology is as follows: 

Since 1 year - Heart Burn

- Recovered without medication

⬇️

7 Months ago - Tuberculosis

- Treated until a month ago, now tested negative

⬇️

Since 9pm that day - Shortness of breath at rest and sweating on exertion

- sudden onset

Patient is a K/C/O Diabetes Mellitus Type 2 Since 12 years and Hypertension since 6 months.

Anatomical location:

As the patient suffered from NSTEMI - Acute Coronary Syndrome  - partial obstruction of a major coronary heart or obstruction of a minor coronary artery completely of the myocardium.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Hypertension - high blood pressure 

2. Type 2 DM - uncontrolled blood sugars 

3. Age 

4. Gender 

REFERENCES:

• https://www.verywellhealth.com/non-st-segment-elevation-myocardial-infarction-nstemi-1746017#:~:text=In%20NSTEMI%2C%20considered%20the%20%22intermediate,damage%20is%20far%20less%20extensive.

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans. The patient was given only the following drug and PCI was not done due to lack of availability.

1.  Tab. MET XL 25 MG/STAT. 

• Metoprolol, Selective Beta 1 receptor blocker.
• Beta blockers reduce myocardial workload, and thus oxygen demand, via a reduction in heart rate and blood pressure. They reduce catecholamine levels, decrease myocardial ischemia and limit infarct size, and may prevent the development of definite infarction in acute coronary syndrome (ACS) patients.
• All hemodynamically stable AMI patients receive BB to reduce chest pain, as well as to reduce the risk of re-infarction and Ventricular arrhythmias. There may be a slight reduction in mortality if the patient has not previously been treated with BB.

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3394111/

3. What are the indications and contraindications for PCI?

Ans. Clinical Indications that could require a percutaneous coronary intervention.

• Acute ST-elevation myocardial infarction (STEMI)
  • Primary PCI is the recommended method of reperfusion when it can be performed in a timely fashion by experienced operators.[1]
  • STEMI and ischemic symptoms of less than 12 hours' duration.[2]
  • STEMI and ischemic symptoms of less than 12 hours' duration and contraindications to fibrinolytic therapy
  • PCI improves survival in patients with significant (>50%) stenosis
• Non–ST-elevation acute coronary syndrome (NSTE-ACS) 
  • Early invasive therapy (within 2 hours of symptoms) recommended with refractory angina, recurrent angina, symptoms of heart failure, new or worsening mitral regurgitation, hemodynamic instability, or sustained ventricular tachycardia/fibrillation.
  • A worsening of troponin levels should trigger an early therapy (within 24 hours)
• Unstable angina
• Stable angina
• Anginal equivalent (e.g., dyspnea, arrhythmia, or dizziness or syncope)
• High-risk stress test findings
• PCI is indicated for the critical coronary artery stenosis, which does not qualify for coronary artery bypass surgery (CABG).

Absolute Contraindications:

• Noncompliance with the procedure and inability to take dual antiplatelet therapy.
• High bleeding risk (thrombocytopenia, peptic ulcer, severe coagulopathy)
• Multiple percutaneous coronary intervention restenosis.

Relative Contraindications:

• Intolerance for oral antiplatelets long-term
• Absence of cardiac surgery backup
• Hypercoagulable state
• High-grade chronic kidney disease
• Chronic total occlusion of SVG
• An artery with a diameter of <1.5 mm
• Stenosis of <50%
• Critical left main stenosis with no collateral flow or patent bypass graft.

REFERENCE:

1. https://www.ncbi.nlm.nih.gov/books/NBK556123/

4. What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on over-testing and overtreatment important to current healthcare systems?

Ans. PCI in stable patients not requiring it was associated with a trend toward higher rates of reinfarction compared with medication therapy. 

• The reinfarctions were not only procedural-related infarcts (i.e., early procedural enzymatic leaks), but true ST elevation reinfarctions that accumulated throughout follow-up. One explanation for the trend toward an increase in reinfarctions with PCI may be embolization resulting in myocardial damage and impaired collateral flow.

Over Diagnosis - An unwanted effect of these developments is over-diagnosis which occurs when a true abnormality is discovered, but detection of that abnormality and its treatment does not benefit the patient.

Over Treatment - The main and worst consequence of over diagnosis is overtreatment of an indolent lesion or disease which is unlikely to have any benefit for the patient. At the same time the likely interventions like surgery, radiation, and chemotherapy can have side effects resulting in significant morbidity and rarely even fatalities can occur.

Cons associated with the above could be:

1. Dangerous side effects due to  over-prescription and over-medicalization.
2. Release of pharmaceuticals into the environment as, for example, in case of over- and misuse of antibiotics, thus contributing to the proliferation of antimicrobial resistance.
3. Psychological effects - unnecessary fear, resulting in increased sense of vulnerability and psychological suffering.
4. Drug Dependence
5. Economic burden - Cost involved in over diagnosis and overtreatment of many diseases will make it difficult to keep healthcare systems financially viable. There is also direct relation between overtreatment and under-treatment, as there is risk of limited resources being redirected and shifted away from those who need them most.

The following approach can be used to prevent any further harm and treat a critical MI patient judiciously.

REFERENCES:

1. https://emcrit.org/pulmcrit/avoiding-over-diagnosis-and-over-treatment-of-mi-in-critically-ill-patients/
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7586591/
3. https://www.acc.org/latest-in-cardiology/clinical-trials/2011/10/30/23/23/oat

NEPHROLOGY

Case 1

https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 1

    1. Why is the child excessively hyperactive without much of social etiquettes ?

Ans. The 8 year old child has the following symptoms suggesting of Attention Deficit Hyperactivity Disorder (ADHD):

• Hyperactive
• Impulsive Behaviour
• Inattentiveness at school
• Excessive fast talking leading to incomprehension of speech

And in association with that, the child also has a Daytime Overactive Bladder wherein the child has the urge to frequently pass urine, almost around 25 times a day, as mentioned by his mother.

It is possible that hence the child experienced the following leading to lack of social etiquettes:

1. Embarrassment associated with the Overactive Bladder.
2. Isolating oneself with gadgets as in this patient, the 8 year old was addicted to smart phone and low self esteem.
3. Lack of social life stemming from lack of interaction with peers and adults, leading to loss of social activities.
4. The child might not notice how his behavior affects other people. He may interrupt a lot and even bug people by breaking social rules.
5. With ADHD sometimes he may lose track of a conversation or get distracted by unrelated thoughts and may also misinterpret what others are saying.
6. The boy can also have trouble with planning and follow-through. That can lead other people to think he can’t be counted on when doing group projects in schools or other activities.

REFERENCES:

• https://www.understood.org/en/learning-thinking-differences/child-learning-disabilities/add-adhd/5-ways-adhd-can-affect-social-skill

    2. Why doesn't the child have the excessive urge of urination at night time ?

Ans. Overactive bladder at night/Nocturia would disrupt the sleep cycle of the child as in this condition he would have frequent urination episodes resulting in waking up more than once from sleep. 

But from history the mother mentions the child having sound and undisturbed sleep.

Following causes of Nocturia are ruled out in this child:

1. Diabetes - Lab Investigations normal, no urine sugars or ketone bodies or any other abnormalities. CUE normal.
2. Medications - Except for occasional constipation medication, no other history of any drug intake.
3. Urinary Tract Infection - No history of UTI, Urine culture and sensitivity negative for microorganisms and showed no growth.
4. Obstructive Sleep Apnea - History of sound and undisturbed sleep
5. Anatomical Abnormality - USG Abdomen normal

REFRENCES:

• https://www.healthline.com/health/overactive-bladder/overactive-bladder-night#takeaway
• https://www.mayoclinic.org/diseases-conditions/bed-wetting/symptoms-causes/syc-20366685

   3. How would you want to manage the patient to relieve him of his symptoms?

Ans. Daytime overactive bladder seen in school aged children as this patient who is 8 years old is distressing and requires timely assessment and management.

1. The goal of evaluation should be to distinguish neurological and anatomical causes from functional causes of bladder dysfunction.
2. A thorough history of voiding symptoms and a Bladder diary are essential components to assessment, directing targeted investigation and treatment. 
3. As all investigations in this child have come out normal, the differential is directing at ADHD, psychosomatic causes or stress related and hence the most common modality for treatment is Behaviour modification and therapy.
4. Behavioural Therapy including:-

•  Reassurance and Relaxation is very important to calm the child and prevent any stressor from triggering this manifestation.  
•  Parenting skills training and Education teaches parents the skills they need to encourage and reward positive behaviors in their children and about various approaches.                  
•  Stress management techniques and Counselling can benefit parents of children with ADHD and the patient by increasing their ability to deal with frustration so that they can respond calmly. 
•  Support groups can help parents and families connect with others who have similar problems and concerns.

      5. Pharmacological management is second line treatment. Behavioural modification should continue throughout treatment.                                                                                    

•  Oxybutynin: Oral. First-line option.                                                                             
•  Ditropan 5 mg Tablets - For 5–12 years, oral, initially 2.5 mg twice daily; if needed, gradually increase to 5 mg 2 or 3 times daily.                                                                  
•  Transdermal route, Oxytrol patch- off label <12 year old can be used if patient can’t swallow or can’t tolerate oral oxybutynin. Do not cut or divide patches as drug release characteristics may be affected.

      6. Treat any associated constipation with diet modification and purgatives/laxatives and treat any other associated infection too.

REFERENCES:

1. https://www.rch.org.au/clinicalguide/guideline_index/Urinary_Incontinence_-_Daytime_wetting/
2. https://www.nimh.nih.gov/health/publications/attention-deficit-hyperactivity-disorder-adhd-the-basics/
3. https://www.stlouischildrens.org/conditions-treatments/pollakiuria

Case 2

https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 2

      1.What could be the reason for his SOB ?

Ans. Urosepsis could be a factor wherein the infection spreads and leads to shortness of breath.

• Hydroureteronephrosis 🠆 retention of urine  🠆 infection with E.coli + presence of pus cells(as detected in investigations)  🠆 urosepsis.

And the patient is also immunocompromised due to his Diabetes.

      2. Why does he have intermittent episodes of  drowsiness ?

Ans. The patient underwent transurethral resection of prostate and could be experiencing drowsiness as a side effect of the procedure as:

• During TURP, the wide plexus of venous sinuses is often opened and the excess absorption of the irrigation fluids which are highly hypotonic into the bloodstream causes a group of symptoms and findings that is called TURP syndrome.
• Absorption of the irrigation fluid (2000 ml or more) used to expand the operating field and to wash away debris and blood, causing hypoosmolality and dilutional hyponatremia may lead to TURP syndrome which could have been the cause for neurological symptoms such as drowsiness and excessive sleep in this patient.
• The symptoms are generally caused by an excessive fluid load in circulation. 

 REFERENCES:

1. https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/transurethral-resection-of-the-prostate-turp
2. https://www.mayoclinic.org/tests-procedures/turp/about/pac-2038488
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4543890/
4. https://pubmed.ncbi.nlm.nih.gov/29424875/
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220352/

      3. Why did he complaint of fleshy mass like passage in his urine?

Ans. Following could be the causes of such visible mass/ foamy passage of the patient's urine:

• Diabetes leading to sediment in urine due to kidney injury.
• Urosepsis/ UTI leading to foamy urine.
• Retrograde ejaculation secondary to TURP as a complication and diabetes as an added factor.
• Dehydration ?
• Proteinuria? due to diabetes and kidney injury

REFERENCES:

1. https://www.healthline.com/health/foamy-urine
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6372866/
3. https://www.nhs.uk/conditions/transurethral-resection-of-the-prostate-turp/risks/

      4. What are the complications of TURP that he may have had?

Ans. Risk factors leading to complications in this patient:

• Prostate size > 45g ( pt's was 60 gm).
• Immunocompromised state due to Diabetes Type 2 diagnosed 5 years back.
• Size of opened venous sinuses?
• Higher absorption of irrigation fluid and usage of excess amounts?
• Longer resection time?
• Bleeding during procedure?
• Excess hypotonic IV fluids administration?

 The patient could have had the following complications following Transurethral Resection of the Prostate:

1. Hyponatremia-TURP syndrome - Due to absorption of excess of irrigation fluid during surgery, leading to fatigue and excessive drowsiness the next day.

NOTE: A technique called Bipolar TURP eliminates the risk of this condition.

1. Acute Tubular Necrosis - Acute Kidney Injury (high risk) due to using distilled water as an irrigant for TURP causing hemolysis, especially in patients with larger prostates as this patient whose prostate was 60g and with longer resection times.
2. Non Oliguric Renal Failure - Due to increasing azotemia (creatinine levels) in this patient (5.2 mg/dl) despite a normal or increased urine output.
3. Post-op Infection - Causing pus cells in urine, raised creatinine.

REFERENCES

• https://www.karger.com/Article/FullText/342965#:~:text=Bacterial%2C%20viral%20or%20fungal%20infections,be%20due%20to%20multiple%20factors.
• https://pubmed.ncbi.nlm.nih.gov/29424875/
• https://pubmed.ncbi.nlm.nih.gov/16863013/
• https://www.goldjournal.net/article/0090-4295(76)90334-4/pdf
• https://www.nhs.uk/conditions/transurethral-resection-of-the-prostate-turp/risks/

GASTROENTEROLOGY

Case 1

https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 1

        1. Which clinical history and physical findings are characteristic of tracheo-esophageal fistula?

Ans. -Tracheo-esophageal fistula (TOF) is defined as a pathological connection between trachea and the esophagus, leading to a spillover of oral and gastric secretions into the respiratory tract.

- It could be associated with various underlying conditions including malignancies, infections, inhalation injuries and traumatic damage spanning multiple organ systems with varying etiologies and acuities.

- Some of the following clinical features of the patient could point to a Tracheo-Esophageal Fistula:

1. Dysphagia 

2. Cough

3. Fever

4. Hoarseness

5. Dyspnea 

6. Weight loss of 10 kgs and malnourished state

- Clinical findings in this patient directing towards a Tracheo-Esophageal fistula:

1. Multiple enlarged necrotic mediastinal lymph nodes - which could be due to TB and lead to erosion into adjacent trachea, bronchi, esophagus.

2. Fistulous communication between left main bronchus and mid thoracic esophagus seen on CECT thorax.

3. Emboli on right descending pulmonary artery seen in CECT Thorax.

4. Enlarged necrotic paraesophageal lymph nodes could also lead to erosion and mass effect.

5. Large opening with proliferative lesion in mid esophagus on endoscopy. 

6. Inspiratory B/L crepts and wheeze heard on examination.

7. Barium swallow finding oustide - could be a fistula.

REFERENCES:

• https://shc.amegroups.com/article/view/5553/html
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896175/

       2. What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

Ans. Immune reconstitution Inflammatory Syndrome:

• It is the paradoxical clinical deterioration attributable to recovery of immune system while receiving highly active antiretroviral therapy (HAART) for the treatment of human immunodeficiency virus (HIV) infection. 
• Deterioration is due to restoration of the patient's capacity to mount an inflammatory immune response against both infectious and noninfectious antigens. 
• Human immunodeficiency virus (HIV) infection is associated with immune activation and depletion of CD4T cells, which leads to defects in immune responses. The use of combination antiretroviral therapy (ART) is associated with repletion of circulating CD4T cells and improvement in immune function, which results in a decrease in the incidence of opportunistic infections. However, some individuals experience clinical disease associated with a prominent inflammatory response to an opportunistic pathogen, such as TB bacteria in this patient after commencing ART.
• A retrospective radiologic review of cases revealed worsening radiographs in 45% of patients with infections like TB having increased lymphadenopathy, lobar consolidations, and pleural effusions.
• The chances of IRIS increase with - Clinical worsening including prolonged fever of >101.5 °F, increasing respiratory symptoms, increasing lymphadenopathy.

            Prevention:

• Infection with tuberculosis 🠆 immune suppression  🠆 reversible with anti-MTB therapy. 

This concept underlies the use of corticosteroids as adjuvant therapy for MTB if a vigorous inflammatory response might compromise vital structures.

• Systemic Corticosteroids have been used in anecdotal reports with good success at preventing further damage when HAART-mediated inflammation threatens vital structures, especially in Tb infection.
• Another intervention is opted to delay the onset of HAART until anti-MTB therapy has decreased the load of organisms. 
• The use of pharmaceutical interventions other than steroids has been limited. Mild cases of inflammation  of TB might respond to nonsteroidal anti-inflammatory drugs (NSAIDs), which could be used by themselves or in conjunction with corticosteroids. 
• The use of other anti-inflammatory therapies, such as thalidomide, is currently being investigated.

NOTE: the most important step is probably to recognize IRIS as a possible explanation for new symptoms as this can help to minimize invasive diagnostic procedures and allow for the early use of therapeutic agents. 

REFERENCES:

1.  https://journals.lww.com/mdjournal/Fulltext/2002/05000/Immune_Reconstitution_Inflammatory_Syndrome_.5.aspx
2. https://err.ersjournals.com/content/29/158/200094
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2813111/

Case 2

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 2

     1. What is the most probable diagnosis in this patient?

Ans. Ruptured Liver Abscess. This seems to be the most probable diagnosis due to the following factors:

• Presenting features of patient - Right hypochondriac pain with symptoms of toxemia including, high grade fever with chills and rigor.
• Laboratory tests indicating impaired liver function - Elevated ALP, Elevated Bilirubin, Hypoalbuminemia, Hypoproteinemia, which have further led to jaundice and pedal edema.
• Could lead to development of spontaneous local peritonitis as a complication, for which characteristic features seen in this patient are - Abdominal Pain, Abdominal distention, Fever, Low urine output, Inability to pass stool or gas, Guarding.
• Presence of a thick collection in right sub-diaphragmatic space could be a sub-diaphragmatic abscess associated with Peritonitis and liver pathology.
• Complete Blood Picture with leukocytosis and neutrophilia also indicate inflammation.

REFERENCES:

1. https://www.mjdrdypu.org/article.aspissn=09752870;year=2017;volume=10;issue=6;spage=532;epage=535;aulast=Bhatia
2. https://bmcsurg.biomedcentral.com/articles/10.1186/s12893-020-00858-w#:~:text=6%2C%2018%5D.-,Spontaneous%20gas%2Dforming%20pyogenic%20liver%20abscess%20(GFPLA)%20is%20a,Previous%20studies%20showed%20that%20E.
3. https://www.mayoclinic.org/diseases-conditions/peritonitis/symptoms-causes/syc-20376247

    2. What was the cause of her death?

Ans. Causes of death could be:

1. Internal bleeding
2. Sepsis 🠊 Shock  🠊  Organ Failure  (following septic peritonitis)
3. Myocardial Ischemia

REFERENCES:

• https://www.hopkinsmedicine.org/health/conditions-and-diseases/peritonitis
• https://www.sciencedirect.com/science/article/abs/pii/S0011393X96800981
• https://jemds.com/latest-articles.php?at_id=10191

    3. Does her NSAID abuse have something to do with her condition? How? 

Ans. Abuse: Exceeding the recommended dosage, taking the drugs for an extended period of time and taking them along with other pain medications for her spine deformity, and taking NSAIDs in combination with toddy occasionally can all increase the risk of stomach or intestinal bleeding, peptic perforation.

• Marie Griffin, MD, professor of preventive medicine at Vanderbilt University, says the risk is considerably higher for older adults, especially for women who frequently take the drugs for persistent pain.
• NSAIDs can reduce the amount of blood reaching the kidneys, slowing kidney function. Water and salt retention, high blood pressure, and electrolyte imbalances have been linked to NSAIDs’ effect on the kidneys. 
•  NSAIDs reduce prostaglandin synthesis, with differences in the extent of inhibition of the enzymes COX-1 and COX-2. Selective COX-2 inhibitors are more likely to cause cardiovascular events, whereas less selective NSAIDs are more likely to cause GI bleeds. 
• NSAIDs reduce the antiplatelet effect of aspirin and have a thrombogenic effect on platelet function.
•  NSAIDs increase systolic blood pressure by 5 mmHg and increase fluid retention.

REFERENCES:

1. https://www.spine-health.com/treatment/pain-medication/potential-risks-and-complications-nsaids#:~:text=Water%20and%20salt%20retention%2C%20high,NSAIDs%20without%20consulting%20a%20doctor.
2. https://www.webmd.com/pain-management/news/20030130/when-relieving-pain-raises-risk

Case 3

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 3

     1. What is causing the patient's dyspnea? How is it related to pancreatitis?

Ans. Breathlessness is the most common symptom of pleural effusion, which has been detected in this patient's Chest X-ray with obliterated/blunting of costophrenic angles. Hence, dyspnea could be due to displacement of diaphragm and inability of chest wall to expand.

 

As the patient has minimal ascites, the cause of shortness of breath (SOB) could be the ascites. The fluid can put pressure on the diaphragm resulting in the lungs being unable to inflate to full capacity and causes SOB.

Relation with pancreatitis:

Interaction between inflammatory events within the pancreas which initiate a generalized systemic inflammatory response. 

Main causes of pleural effusion in a patient with pancreatitis are:

• Trans-diaphragmatic lymphatic blockage
• There may be a disruption of pancreatic duct, leading to the leakage of pancreatic enzymes and the formation of a pancreatico-pleural fistula, more likely to occur if the duct disruption is posteriorly into the retroperitoneum.
• The pancreatic-pleural fistulae secondary to leak and disruption of the pancreatic duct or pseudocyst caused by an episode of acute pancreatitis. The pancreatic enzymes can track up into the mediastinum and then rupture into the pleural cavity either left side or bilaterally and so create a connection between the pancreatic duct and the pleural cavity.
• Exudation of fluid into the pleural cavity from the subpleural diaphragmatic vessels may also cause pleural effusion.

REFERENCES:

1. https://www.scitechnol.com/peer-review/an-unusual-case-of-dyspnoea-in-a-patient-with-chronic-liver-disease-qeSr.php?article_id=7559
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5633324/
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386740/

     2. Name possible reasons why the patient has developed a state of hyperglycemia.

Ans. Part of endocrine function of pancreas could be affected in acute pancreatitis resulting in Stress Hyperglycemia in this acute phase. 

It could be due to any of the following reasons:

1. One factor could be because of the sympathetic hyperactivity and circulating catecholamines that elevate glucagon.
2. Due to microcirculation disorder and inflammation resulting in pancreas edema, ischemia and necrosis hence affecting secretion and excretion of insulin due to damage to Langerhans Islet cells.
3. Due to acute metabolic stress similar to that seen in other clinical situations such as sepsis.
4. Thus hyperglycemia could hence be the result of a hyperglucagonemia secondary to stress or the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells 

In summary, relative hypoinsulinemia and hyperglucagonemia probably are, together with the elevated levels of catecholamines and cortisol, the most important factors involved in the pathogenesis of hyperglycemia observed during acute pancreatitis.

REFERENCES:

1. https://link.springer.com/chapter/10.1007/978-3-642-60580-2_11
2. https://clinicaltrials.gov/ct2/show/NCT01470885

     3. What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

Ans. Chronic Alcohol consumption seems to be the primary cause leading to pancreatitis in this patient resulting in increased manufacture of lipase and destructive lysosomes by the pancreas, as well as sensitization of the pancreatic cells to naturally occurring chemicals, such as cholecystokinin, which may further activate pancreatic enzymes, thus resulting in:

• Lipase - 118 IU/L  
• Amylase - 252 IU/L 

Note: Both the above enzymes are markedly elevated.

Liver is the chief organ responsible for the metabolism of alcohol and hence in chronic consumption of alcohol as in this patient, the liver is the primary site vulnerable to alcohol induced injury thus resulting in elevated liver enzymes and abnormal liver function tests.

Diagnosis of Alcoholic Fatty Liver Disease (AFLD) typically relies on laboratory tests for biomarkers of liver enzymes and laboratory factors for definite diagnosis of AFLD are as follows:

• Elevated levels of gamma glutamyl transferase (GGT), aspartate aminotransferase (AST), and alanine aminotransferase (ALT).
• If the AST level is more than that of ALT, a AST/ALT ratio of  > 1 some studies have found in more than 80 percent of alcoholic liver disease patients.
• Neutrophilia
• Increased Bilirubin levels

Note: Of the above mentioned markers, an AST/ALT ratio > 1.5 has been considered specific for AFLD.

REFERENCES

1. https://www.journal-of-hepatology.eu/article/S0168-8278(18)32576-5/fulltext#secst095
2. https://pubs.niaaa.nih.gov/publications/aa64/aa64.htm

     4. What is the line of treatment in this patient?

Ans. Management in this patient is aimed at:

Bed Rest

Intravenous Support

Pain control/Analgesia

Antiemetic

Prophylactic Antibiotics

Hydration

 Maintaining Adequate Nutrition

 Prevention/Control of Complications

Lifestyle changes to reduce alcohol consumption

Note: Further GRBS Charting to be done to keep the hyperglycemia in check and in case Diabetes diagnosed, oral antidiabetic drugs to be administered. 

- The physiologic stress of acute pancreatitis results in hyper-metabolism, thus creating increased nutritional needs.

- Any further complications such as hypovolemia, nausea/vomiting, ards, infection, DIC should be prevented.

REFERENCES:

1. https://www.sciencedirect.com/science/article/abs/pii/S1521691803000507
2. https://www.clinicaladvisor.com/home/features/what-you-should-know-about-acute-pancreatitis/

Case 4

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 4

     1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans.  The evolution of the symptomatology is as follows: 

5 Years ago - Abdomen Pain + Vomiting

- Local hospital, treated conservatively

⬇️

Asymptomatic next 3 years

⬇️

Recurrent episodes of pain abdomen and vomiting

- Post resuming alcohol consumption 2 years back

⬇️

Past 1 year, Abdomen pain + Vomiting

- 5 to 6 episodes, Local RMP treated

⬇️

Increased alcohol intake since past 20 days 

- 5 bottles of toddy per day

⬇️

Past 1 Week, Pain Abdomen and Vomiting 

- throbbing, left umbilical-hypochondriac-lumbar-hypogastrium

- non bilious, non projectile 

⬇️

Since 4 Days - Fever

- High grade, continuous and with chills and rigors

⬇️

Since 4 Days - Constipation

- Passing flatus

⬇️

Since 4 Days - Burning Micturition

- With Suprapubic pain, increased frequency and urgency

⬇️

Later, patient developed - Progressive Pneumothorax

- during hospital stay

Anatomical location:

• Based on the CECT, the site of abnormality is the abdomen - pancreas behind the peritoneum of posterior abdominal wall , where the pseudocyst is located due to chronic pancreatitis of the pancreas.
• Pleural effusion between tissues lining the chest-wall and lungs
• Pneumothorax in the space between lungs and chest wall.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Consumption of Increased alcohol (Toddy) 🠆 Recurrent sudden episodes of acute pancreatitis on chronic pancreatitis, leading to complications 🠆 Pseudocyst formation.

2. Infection of pancreas ?

3. Pancreatic injury? trauma?

 

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653285/

    2. What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would you approach this patient as a treating physician?

Ans. Efficacy of the interventions:

• Oxygen Supply - For mild Hypoxia 

• Inj. MEROPENEM TID for 7 days - Broad Spectrum Antibiotic 

1. Meropenem is as effective as imipenem in preventing septic complications of patients with severe acute pancreatitis.

• Inj. METROGYL 500 mg IV TID for 5 days - Antibiotic

1. Systemic Metronidazole is indicated for the treatment of many anaerobic infections which can clinically present

• Inj. AMIKACIN 500 mg IV BD for 5days - Antibiotic 

1. The use of prophylactic antibiotics in severe alcoholic acute pancreatitis significantly reduces the incidence of severe infection.

• Total Parenteral Nutrition - Feeding Bypassing GI Tract

1. Prevents malnutrition and is a key to reduce inflammation, complications and death in acute pancreatitis. It is considered in patients who cannot tolerate enteral nutrition.
2. All pancreatic fistulae that developed during the course of the disease spontaneously closed in patients receiving TPN without operation in a mean period of 33.3 days, and all pseudocysts subsided in an average of 18.3 days. 

• I.V NS / RL at the rate 12l ml per hour - Fluid replacement for dehydration

1.  Normal saline (NS) or Ringer’s lactate (RL) may improve mortality rates and decrease development of systemic inflammatory response syndrome (SIRS), especially the latter.

• Inj. OCTREOTIDE 100 mg SC/BD - Somatostatin analogue

1. Long-acting analogue of Somatostatin, Octreotide is a potent inhibitor of exocrine secretion of the pancreas, which plays an important role in the pathogenesis of acute pancreatitis. They also have direct anti-inflammatory and cyto-protective effects.

• Inj. THIAMINE 100 mg in 100 ml NS  IV/TID - Prophylactic B1 supplementation

1. To prevent Wernicke encephalopathy secondary to thiamine deficiency.

• Inj. TRAMADOL in 100 ml NS  IV/OD -  Opioid Analgesic

1. Tramadol is the most effective oral opioid analgesic for reducing pain in chronic pancreatitis

• PANTOP 40 mg IV/OD - Proton Pump Inhibitor

1. Pantoprazole as a proton pump inhibitor (PPI) has pancreatic anti-secretory effect and a pronounced inhibitory reactivity towards hydroxyl radicals. 

• USG guided Malecot drainage - For peri pancreatic fluid 

1. Decreased mortality, high success rate and less adverse events rate.

• Intercostal drainage - Pneumothorax 

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1458598/
2. https://pubmed.ncbi.nlm.nih.gov/14576501/#:~:text=Meropenem%20is%20as%20effective%20as,patients%20with%20severe%20acute%20pancreatitis.
3. https://www.hindawi.com/journals/hpb/2010/523468/#conclusion
4. https://pubmed.ncbi.nlm.nih.gov/1903137/
5. https://pubmed.ncbi.nlm.nih.gov/8829189/
6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7211526/
7. ournals.lww.com/ajg/fulltext/2018/10001/ringer_s_lactate_vs_normal_saline_in_acute.2.aspx#:~:text=Normal%20saline%20(NS)%20is%20the,poor%20outcomes%2C%20compared%20to%20NS.
8. https://www.medscape.com/viewarticle/487410#:~:text=Somatostatin%20and%20its%20long%2Dacting,anti%2Dinflammatory%20and%20cytoprotective%20effects.
9. https://pubmed.ncbi.nlm.nih.gov/22233960/
10. https://www.aafp.org/afp/2008/0301/p661.html#:~:text=There%20is%20consensus%20that%20tramadol,associated%20with%20gastrointestinal%20adverse%20effects.
11. https://pubmed.ncbi.nlm.nih.gov/23242019/#:~:text=Pantoprazole%20as%20a%20proton%20pump,the%20course%20of%20acute%20pancreatitis.
12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4735000/

Approach to patient:

1. Detailed History Taking

- Chief complaints, Lifestyle habits and personal history, Treatment history

🠋

2. Clinical Examination

- Vitals, General and Systemic Examination (inspection, palpation, percussion, auscultation)

🠋

3. Routine Laboratory Investigations

- CBP, CUE, LFT, RFT, ABG, Serum amylase and lipase, Pleural Tapping

🠋

4. Special Investigations

- Chest X-ray, CECT scan

🠋

5. Microbiology / Pathology

- Culture & sensitivity, serology

🠋

6. Treatment Modalities

                                                     ↙                                                        ↘

                                            Conservative                                         Non Conservative

                                         - Prophylactic Antibiotics               - USG guided percutaneous drainage

                                         - Analgesics, antipyretics                - Intercostal Drainage   

                                         - Antiemetics

                                         - Proton Pump Inhibitor

                                         - Bed Rest and oxygen support

                                         - Intravenous Support with fluids and hydration

                                         - Maintaining Adequate Nutrition and Vitamin supplementation

 

NOTE: - Prevention/Control of Complications.

              - Lifestyle changes to reduce alcohol consumption.

HEPATOLOGY

Case 1

https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 1

        1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it? What could be the cause in this patient?

Ans. Yes, Indigenously brewed alcohol could be the cause for liver abscess in this patient as he has a history of chronic Toddy intake -1 bottle per day for the last 30 years.

Contributory factors for causation of liver abscess in this patient could be as follows:

• Male gender.
• Manual laborer - Palm tree climber.
• Tobacco Beedi smoking.
• Socio-economic background 
• Lifestyles practices predisposing to high parasitic burden.

Toddy related factors could be as follows:

• Relatively lower percentage of alcohol (<5%)
• Possibility of microbial contamination due to a lack of distillation process.
• Microbial or parasitic contamination, transmission and infection during preparation and storage of toddy.
• The nonalcoholic content of toddy alters the gut environment and upregulating enzymes, switching latent Entamoeba (EH) to virulence.
• High iron content in Toddy promotes growth and in-vivo invasiveness of EH, an etiological agent in liver abscess causation. 

 REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/
2. https://onlinelibrary.wiley.com/doi/full/10.1002/jgh3.12137

            

        2. What is the etio-pathogenesis of liver abscess in a chronic alcoholic patient ? (since 30 years - 1 bottle per day)

Ans. Etio-pathogenesis:

• Possible route of spread - Portal transmission or Hematogenous spread or direct spread from biliary system.
• Possible pathology - Bowel content leakage and peritonitis or any intra abdominal infections.

                                            Bacteria travel   ╍╍via portal vein╍╍>  Liver

 

                                          - Generalized septicemia ( infection from anywhere else in the body).

                                            Bacteria travel   ╍╍via hepatic artery╍╍>  Liver

• Makkar et al. have suggested that high iron content of traditional fermented beverages and iron overload due to chronic alcoholism could also lead t
• A high microbial burden due to poor sanitation and immunosuppressive effects of alcohol could render the host more vulnerable to infections. Thus, both the host factors as well as contents of toddy may be responsible for the pathogenesis of liver abscess. 

 REFERENCES:

1. https://www.worldwidejournals.com/indian-journal-of-applied-research-(IJAR)/recent_issues_pdf/2016/October/October_2016_1492168550__175.pdf
2. https://www.researchgate.net/publication/250212621_Pyogenic_Liver_Abscess_and_Indigenous_Alcohol
3. https://www.ijph.in/article.aspissn=0019557X;year=2019;volume=63;issue=1;spage=89;epage=90;aulast=Kumar#:~:text=Amoebic%20liver%20abscess%20(ALA)%20is,and%20the%20occurrences%20of%20ALA.&text=Toddy%20is%20a%20local%20alcoholic%20beverage%20consisting%20of%20fermented%20palm%20juice.

          3. Is liver abscess more common in right lobe ?

Ans. 50% of solitary liver abscesses occur in the right lobe of the liver as it is a more significant part with more blood supply.

Anatomical considerations:

- The right lobe is supplied by the hepatic artery and the portal vein.

- Right lobe is also predominantly supplied by superior mesenteric vein.

- Right lobe has denser network of biliary canaliculi. 

- Most of the hepatic volume is in the right lobe as compared to left lobe and caudate lobe.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/books/NBK538230/#:~:text=50%25%20of%20solitary%20liver%20abscesses,liver%20lobe%20or%20caudate%20lobe.

       4. What are the indications for ultrasound guided aspiration of liver abscess ?

Ans. Percutaneous ultrasound-guided needle aspiration is a safe diagnostic and therapeutic approach which enhances clinical recovery. 

-Indications for Aspiration in this patient could be follows:

• Abscess size of 9.7 x 9.4.
• Clinical deterioration - Elevation of ALP, transaminases, Bilirubin and Low Albumin signifying impaired liver function. 
• To test the culture and antibiotic sensitivity and identify the causative organism.
• Failure of clinical improvement of symptoms.

REFERENCES:

1. https://surgical.medresearch.in/index.php/ijoso/article/view/88/176

Case 2

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 2

      1. Cause of liver abscess in this patient ?

Ans. The possible causes in this patient could be:

• Ingestion of contaminated food or water.
• Toddy consumption.
• Male gender having higher occurrence.
• Lifestyle or hygienic practices.

      2. How do you approach this patient ?

Ans. The patient should be approached in the following manner:

1. Detailed History Taking

- Chief complaints, Lifestyle habits and practices, Medical history, Travel history.

🠋

2. Clinical Examination

- Vitals, General and Systemic Examination (inspection, palpation, percussion, auscultation)

🠋

3. Routine Laboratory Investigations

- CBP, CUE, LFT, RFT

🠋

4. Special Investigations

- Chest X-ray, Ultrasonography, CT scan, MRI

🠋

5. Microbiology / Pathology

- Culture & sensitivity, serology

🠋

6. Treatment Modalities

                                                     ↙                                                        ↘

                                            Conservative                                         Non Conservative

                                         - Antibiotics                      - USG guided aspiration and percutaneous drainage

                                         - Analgesics                      - Open surgical Drainage 

                                         - Antipyretics

                                         - Multivitamin Supplements

     

      NOTE: In this patient, pus was self-resolving, symptoms subsided in response to medical treatment and hence to avoid any further complications, aspiration was avoided. 

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3014521/

       

        3. Why do we treat here: both amoebic and pyogenic liver abscess? 

Ans. The patient was treated simultaneously for both pyogenic and amoebic liver abscess:

1. Inj. ZOSTUM 1.5 gm IV BD: Zostum is a combination medicine of 2 Antibiotic drugs - Sulbactam (penicillin) and Cefoperazone (cephalosporin) to treat Bacterial Infection.
2. Inj. METROGYL 500mg IV TID: Metrogyl is an anti-infective medicine comprising of an Antibiotic Metronidazole to treat Bacterial/Parasitic Infections (Amoebic).

Rationale Behind This Treatment Modality:

• The clinical presentation of both Amoebic and Pyogenic Liver Abscess is indistinguishable. 
• Patients usually present with fever and right upper quadrant tenderness.
• Laboratory tests abnormalities such as in this patient showing leukocytosis, increased alkaline phosphatase (ALP) and abnormal liver and renal function tests are often present in both and cannot differentiate effectively. 
• Even, imaging techniques, such as ultrasonography and computed tomography (CT) scanning, are useful in demonstrating a space occupying lesion and confirm only the presence or absence of a liver abscess but may not reliably differentiate between PLA and ALA. 

Hence, Antimicrobial Empiric Therapy targeting both amoebic and pyogenic causes of liver abscess is recommended. As treatment is often administered prior to collection of appropriate specimens, the causative pathogen and prevalence of either disease remains unclear.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/books/NBK430832/
2. https://academic.oup.com/bmb/article/132/1/45/5677141

         4. Is there a way to confirm the definitive diagnosis in this patient?

Ans. Many possible methods have been employed in reaching a definite diagnosis as follows:

• Fine needle aspiration for culture is the gold standard for diagnosis of PLA(pyogenic).
• Blood cultures, Entamoeba serology, liver abscess aspirate for culture, molecular and antigen testing also help in reaching a definite diagnosis.
• New potential marker such as Pyruvate Phosphate Dikinase in the form of a lateral flow assay shows potential in the diagnosis of ALA (amoebic).
• Presumptive diagnoses of amoebic (n=471; 82%) vs. pyogenic (n=106; 18%) abscess were based upon amoebic serology, microbiological culture results, and response to therapy.
• Patients with amoebic abscess were more likely to be young males with a tender, solitary, right lobe abscess (P=0.012).
• Univariate analysis found patients with pyogenic abscess more likely to be over 50 years old, with a history of diabetes and jaundice, with pulmonary findings, multiple abscesses, amoebic serology titres <1:256IU and lower levels of serum albumin (P<0.04). 
• Multivariate logistic regression analysis confirmed that age >50 years, pulmonary findings on examination, multiple abscesses, and amebic serology titres <1:256IU were predictive of pyogenic infection.

REFERENCES:

1. https://academic.oup.com/bmb/article/132/1/45/5677141
2. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-3156.2004.01246.x

PULMONOLOGY

Case 1

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 1

        1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient's problem?

       Ans. The evolution of the symptomatology is as follows: 

20 Years ago - Shortness of Breath (intermittent)

- 1st episode, 1 week long, January, grade 2

⬇️

Next 8 years till 12 years ago, every year - Shortness of breath (SOB)

- 1 week long episode, January, grade 2

⬇️

12 Years ago - Shortness of Breath

- 20 days long episode, grade 2

⬇️

Every year 1 episode of SOB since 12 years

- 1 month long episode, grade 2

⬇️

8 Years ago - Diabetes Mellitus diagnosed 

⬇️

5 years ago - Anemia 

⬇️

1 Month back - General Weakness 

⬇️

30 Days ago - Latest episode of SOB

- gradual progression, insidious onset

- started as grade 2

⬇️

20 Days ago - Bronchiectasis Diagnosed

⬇️

20 Days ago - Hypertension Diagnosed

⬇️

15 Days ago - Pedal edema post empirical ATT

⬇️

15 Days ago - Facial puffiness post empirical ATT

⬇️

2 Days ago - Drowsiness

⬇️

2 Days ago - SOB progressed to Grade 4

⬇️

2 Days ago - Decreased urine output

Anatomical location:

Based on the X-ray picture, the site of abnormality is the para-cardiac area of right lung.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Exposure to rice dust, pesticides in soil or allergens in the work environment as the patient experienced symptoms primarily during January when she worked in the paddy fields.

2. Exposure to microorganisms such as Moraxella catarrhalis, H. Influenza, Pneumococcus, Viral agents etc. and thus subsequent infections.

      

      2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

      Ans.  Tab Zoryl 

                      • Mechanism of Action:

- Zoryl 1 MG Tablet is a long-acting oral anti-diabetic which lower the blood sugar level.

- Glimiperide is a sulfonylurea and acts as an insulin secretagogue. It lowers blood sugar by stimulating the release of insulin by pancreatic beta cells and by inducing increased activity of intracellular insulin receptors.

-At the molecular level, Metformin inhibits the mitochondrial respiratory chain in the liver, leading to activation of AMPK, enhancing insulin sensitivity (via effects on fat metabolism) and lowering cAMP, thus reducing the expression of gluconeogenic enzymes. Hence, inhibition of hepatic gluconeogenesis.

                      • Therapeutic Indications:

- Type 2 diabetes mellitus in the patient.

                      • Efficacy over Placebo:

- Metformin improved glucose variables as compared with placebo. 

- Metformin lowered fasting plasma glucose and HbA1c generally in a dose-related manner. 

              Tab Telma

                       • Mechanism of Action:

- Each tablet contains 40 mg Telmisartan.

- Telmisartan is an orally active and specific angiotensin II receptor (type AT1) antagonist. Telmisartan displaces angiotensin II with very high affinity from its binding site at the AT1 receptor subtype.

                       • Therapeutic Indications:

- Essential Hypertension.

- Reduction of cardiovascular morbidity in this patient with type 2 diabetes mellitus.

                      • Efficacy over Placebo:

- Telmisartan efficacy was defined as significant decrease in SBP at day 14 compared to placebo and a clinically relevant (>20 mm Hg) decrease in SBP at day 28.

                BIPAP

                      • Mechanism of Action:

- Bilevel positive airway pressure.

It is a type of ventilator, a device that helps with breathing. A BiPap machine can help push air into your lungs. You wear a mask or nasal plugs that are connected to the ventilator. The machine supplies pressurized air into your airways. It is called “positive pressure ventilation” because the device helps open your lungs with this air pressure.

                     • Therapeutic Indications 

- Chronic obstructive pulmonary disorder (COPD)

                   

               Lasix - Furosemide

                         • Mechanism of Action:

- Loop diuretic. Acts by inhibiting reabsorption of sodium and chloride ions at proximal and distal renal tubules and loop of Henle, by interfering with chloride-binding cotransport system, causes increases in loss of water, calcium, magnesium, sodium and chloride.

                         • Therapeutic Indications

- Edema, Hypertension.

- 2D echo suggesting right heart failure

                         • Efficacy over Placebo:

- Furosemide is the choice of drug for loop diuretic therapy in heart failure.

                Azithromycin

                          • Mechanism of Action:
-Binds to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest and does not affect nucleic acid synthesis.
                          • Therapeutic Indications:
- Acute exacerbation of COPD due to possible infectious etiology.
                          • Efficacy over Placebo:
- COPD, azithromycin taken daily for 1 year, when added to usual treatment, decreased the frequency of exacerbations and improved quality of life.

                   Augmentin

                           • Mechanism of Action:
- Amoxicillin binds to penicillin-binding proteins, thus inhibiting final transpeptidation step of peptidoglycan synthesis in bacterial cell walls and addition of clavulanate inhibits beta-lactamase-producing bacteria, allowing amoxicillin extended spectrum of action.

- It is a semisynthetic antibiotic with a broad spectrum of bactericidal activity, covering both gram-negative and gram-positive microorganisms.

                           • Therapeutic Indications:
- For possible infectious etiology of COPD.

                           • Efficacy over Placebo:
- Patients with exacerbations of mild to moderate COPD have a higher rate of cure when given amoxicillin/clavulanate compared with placebo.

                  Oxygen Inhalation

                             • Therapeutic Indications:
- Patient's oxygen saturation was 75% at room air.

                             • Efficacy over Placebo:

- Restores oxygen reserves in tissues.

                  Chest physiotherapy

                             • Mechanism of Action: 

- Intermittent positive pressure ventilation and positive expiratory pressure were effective in improving sputum expectoration. In addition, walking programmes led to benefits in arterial blood gases, lung function, dyspnoea and quality of life for patients with exacerbation.
- Chest physiotherapy involves a number of physical techniques to help remove excess mucus from respiratory passages and improve breathing. The goal is to help patients breathe more freely and get more oxygen through the blood stream into all parts of the body. Normally, mucus helps lubricate the lungs.

                              • Therapeutic Indications:
- Dyspnea in patient due to COPD.

                     HAI- Human Actrapid Insulin

                             • Mechanism of Action: 

- Actrapid is human insulin with a fast-acting effect by inhibiting glucose output by liver.

                             • Therapeutic Indications:

- Actrapid is used to reduce the high blood sugar level in this patient with diabetes mellitus.

                     Nebulization with:-

1. IPRAVENT respules is indicated as a bronchodilator for the maintenance treatment of bronchospasm and dyspnea associated with acute exacerbation chronic obstructive pulmonary disease (COPD) in this patient.
Ipratropium bromide is an anticholinergic with para-sympatholytic properties. Anticholinergics prevent the increase in intracellular concentration of cyclic guanosine monophosphate (cyclic GMP) caused by the interaction of acetylcholine with the muscarinic receptors on bronchial smooth muscle.

2. BUDECORT respules contains the potent, non-halogenated, corticosteroid, indicated for dyspnea in this patient due to COPD and to inhibit inflammatory cytokine production.
Budesonide is the potent topical anti-inflammatory glucocorticoid that controls these symptoms.

     3. What could be the causes for her current acute exacerbation?

Ans. Exacerbations of COPD are thought to be caused by complex interactions between the host, bacteria, viruses, and environmental pollution. These factors increase the inflammatory burden in the lower airways, overwhelming the protective anti‐inflammatory defences leading to tissue damage.
Aspen workshop7 defined AECOPD as “a sustained worsening of the patient's condition from the stable state and beyond normal day to day variations, that is acute in onset and necessitates a change in regular medication in a patient with underlying COPD”.

1. Respiratory infections including bacteria, atypical organisms and respiratory viruses, 10% are due to environmental pollution.
2. Dust exposure in the working environment affects the lung function values and increased the respiratory symptoms among the rice mill workers and patient works in paddy fields.
3. Cooking using solid fuels (such as wood, crop wastes, charcoal, coal and dung) and kerosene in open fires and inefficient stoves. And the patient has been using chulha for past 20 years. One in four or 25% of deaths from chronic obstructive pulmonary disease (COPD) in adults in low- and middle-income countries are due to exposure to household air pollution. Women exposed to high levels of indoor smoke are more than twice as likely to suffer from COPD than women who use cleaner fuels and technologies.

          4. Could the ATT have affected her symptoms, if yes, how?

Ans. - Rifampicin and Isoniazid causes muscle weakness and hence could have been a factor leading to generalized weakness.

         - Rifampicin is highly protein bound, can cause hypoalbunimea, which could have lead to decreased oncotic pressure, further leading to fluid accumulation in interstitium of dependant parts causing pedal edema. 

           5. What could be the cause for electrolyte imbalance? 

Ans.  

•  As the patient received LASIX - Furosemide treatment, it could have led to fluid or electrolyte imbalance (hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia or hypocalcemia) and she showed the respective signs of electrolyte imbalance : weakness, lethargy, drowsiness, muscular fatigue, oliguria.
• Corticosteroids (Includes hydrocortisone) which the patient was administered and could have caused electrolyte imbalance due to mineralocorticoid functions. Corticosteroids can cause hypokalemia and fluid retention.
• As the patient has right heart failure, this may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympatho-adrenergic stimulation), and due to the complications of therapy with diuretics, etc. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function. 

 REFERENCES CASE 1:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2080749/#!po=20.5556

2. https://erj.ersjournals.com/content/29/6/1224

3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019758/

4. https://www.google.com/url?sa=t&source=web&rct=j&url=https://e-journal.unair.ac.id/JR/article/download/20435/12292%23:~:text%3DRice%2520dust%2520is%2520easily%2520exposed,dust%2520syndrome%252C%2520and%2520hypersensitivity%2520pneumonitis.&ved=2ahUKEwiKxeL_puLwAhXRzjgGHUZiCswQFjABegQIBBAG&usg=AOvVaw0n-RRD5OjZNRoKpp6SUyVg

5. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0231757

6. https://www.who.int/news-room/fact-sheets/detail/household-air-pollution-and-health

7. https://reference.medscape.com/drug/zithromax-zmax-azithromycin-342523#0

8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1113909/  

9. https://scholar.google.co.in/scholar?q=Azithromycin+in+copd+and+placebo&hl=en&as_sdt=0&as_vis=1&oi=scholart#d=gs_qabs&u=%23p%3DbzW84WHZDqAJ 

10. https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464645/%23:~:text%3DSubjects%2520with%2520heart%2520failure%2520may,the%2520development%2520of%2520cardiac%2520arrhythmias.&ved=2ahUKEwjg2vO4yuLwAhVRSX0KHb_VCdIQFjABegQIBBAF&usg=AOvVaw2F_VXqcnXx9ZIT-tMh5E5x

11. https://pubmed.ncbi.nlm.nih.gov/1507935/

12. https://www.rxlist.com/lasix-drug.htm#:~:text=All%20patients%20receiving%20LASIX%20therapy,pains%20or%20cramps%2C%20muscular%20fatigue%2C

13. https://www.drugs.com/disease-interactions/hydrocortisone.html#:~:text=Corticosteroids%20(Includes%20hydrocortisone)%20electrolyte%20imbalance&text=Corticosteroids%20can%20cause%20hypernatremia%2C%20hypokalemia,then%20by%20prednisone%20and%20prednisolone

14. https://www.aafp.org/afp/2013/0401/p512.html

15. https://reference.medscape.com/drug/augmentin-amoxicillin-clavulanate-342474#10

16. https://reference.medscape.com/drug/lasix-furosemide-342423#0

17. https://pubmed.ncbi.nlm.nih.gov/30851066/#:~:text=Telmisartan%20efficacy%20was%20defined%20as,in%20SBP%20at%20day%2028.&text=Conclusions%20and%20clinical%20importance%3A%20Telmisartan,well%20tolerated%20in%20hypertensive%20cats.
    

18. https://www.medicines.org.uk/emc/product/5386/smpc#gref 

19. https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/bipap%3Famp%3Dtrue&ved=2ahUKEwi2vI6NteLwAhXJF3IKHbpAAcgQFjABegQIBBAG&usg=AOvVaw1xOS9tUx5asuxlsJdgRGqx&ampcf=1&cshid=1621862794869

20.  https://www.google.com/amp/s/www.practo.com/medicine-info/amp/zoryl-1-mg-tablet-12322

21. https://www.ciplamed.com/content/budecort-respules

22. https://www.ciplamed.com/content/ipravent-respulesrespirator-solution#pharmacological%20properties 

23. http://rc.rcjournal.com/content/59/10/1583#:~:text=Head%20of%20bed%20elevation%20(HOBE,improve%20oxygenation%20and%20hemodynamic%20performance. 

24. https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.oleanpt.com/library/4306/ChestPhysiotherapy.html&ved=2ahUKEwjSj6DzuuLwAhUY4zgGHXjRD6sQFjAEegQIIBAF&usg=AOvVaw2wFytBRnfdVPOd9x1TuHao

25. https://www.sciencedirect.com/science/article/abs/pii/S0031940609000868

26. https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.utmb.edu/policies_and_procedures/4230160%23:~:text%3DDiseases%2520frequently%2520requiring%2520postural%2520drainage,COPD%252C%2520bronchitis%252C%2520lung%2520abscess.%26text%3Dpleural%2520effusion%252C%2520anxiety%252C%2520angina.%26text%3DUndiagnosed%2520chest%2520pain.%26text%3DPulmonary%2520edema%252C%2520congestive%2520heart%2520failure.&ved=2ahUKEwjSj6DzuuLwAhUY4zgGHXjRD6sQFjACegQIBRAG&usg=AOvVaw2hxt65oLP0t_oUhYA_zoKW

27. https://en.m.wikipedia.org/wiki/Glimepiride
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5552828/
    https://pubmed.ncbi.nlm.nih.gov/9428832/#:~:text=Results%3A%20Metformin%20improved%20glucose%20variables,to%202000%20mg%20daily%2C%20respectively

NEUROLOGY

Case 1

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 1

1. Does the patient's history of road traffic accident have any role in his present condition?

Ans. As the patient had injury to shoulder and head & neck - Zygomatic process, Mandibular process, it is possible that the trauma due to the RTA could have been a risk factor to the occurrence of the CVA.

• It could be due to a fracture or trauma leading to a tear in the head or neck blood vessels that lead to the brain, which can be a source of blood clots that cause a stroke.

REFERENCE: https://www.sciencedaily.com/releases/2014/02/140213184804.htm

2. What are warning signs of CVA?

Ans. The warning signs of a Cerebrovascular Accident could be as follows:

1. Sudden NUMBNESS or WEAKNESS of face, arm, or leg, especially on one side of the body.
2. Sudden CONFUSION, trouble speaking or understanding speech.
3. Sudden TROUBLE SEEING in one or both eyes.
4. Sudden TROUBLE WALKING, dizziness, loss of balance or coordination.
5. Sudden SEVERE HEADACHE with no known cause.

Note: Act F.A.S.T. and do the following simple test:

F—Face: Ask the person to smile. Does one side of the face droop?
A—Arms: Ask the person to raise both arms. Does one arm drift downward?
S—Speech: Ask the person to repeat a simple phrase. Is the speech slurred or strange?
T—Time: If you see any of these signs, call 9-1-1 right away.

REFERENCES:

1. https://www.stroke.org/en/about-stroke/stroke-symptoms
2. https://www.cdc.gov/stroke/signs_symptoms.htm

3. What is the drug rationale in CVA?

Ans. “Time is brain”—following middle cerebral artery (MCA) occlusion, irreversible ischaemic brain damage evolves over hours. Reperfusion can rescue tissue which is functionally inactive but still viable (the “ischemic penumbra”).

The following drugs were used in this patient:

1. Mannitol

• Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
• Mannitol decreases elevated intracranial pressure after stroke and results in increased cerebral perfusion pressure and brain oxygenation in large, hemispheric strokes.
• Reference: ://www.ahajournals.org/doi/pdf/10.1161/01.str.0000078658.52316.e8

2. Atorvastatin

• The beneficial effect of statin therapy on the risk of recurrent stroke was due to a reduction in the risk of cerebral infarction, the mechanism of which largely has been attributed to a reduction in LDL cholesterol levels. The lower average LDL cholesterol level achieved in the atorvastatin as compared with the placebo group is consistent with this hypothesis. 
• Decreased the risk of stroke, major coronary events, and revascularization procedures. These results support the initiation of atorvastatin treatment soon after a stroke or TIA.
• Statins lower serum cholesterol level by inhibiting hydroxymethylglutaryl-coenzymeA (HMG-CoA) reductase. Statins have been found to improve endothelial function, modulate thrombogenesis, attenuate inflammatory and oxidative stress damage, and facilitate angiogenesis far beyond lowering cholesterol levels . Statins have also been proved to significantly decrease cardiovascular risk and to improve clinical outcome.
• References: - https://www.nejm.org/doi/10.1056/NEJMoa061894#:~:text=In%20conclusion%2C%20in%20patients%20with,after%20a%20stroke%20or%20TIA.
  - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428028/

3. Ecosprin - Aspirin

• Aspirin, which thins the blood and thereby prevents clots, is currently used to reduce the long-term risks of a second stroke in patients who've had an ischemic stroke.
• Aspirin slows the blood's clotting action by reducing the clumping of platelets. Platelets are cells that clump together and help to form blood clots. Aspirin keeps platelets from clumping together, thus helping to prevent or reduce blood clots.
• During a heart attack, blood clots form in an already-narrowed artery and block the flow of oxygen-rich blood to the heart muscle (or to part of the brain, in the case of stroke).
• References:

1. https://www.webmd.com/stroke/news/20000601/aspirin-after-stroke-helps-prevent-another
2.  https://www.uofmhealth.org/health-library/te7903spec

Vital signs, while nonspecific, can point to impending clinical deterioration and hence should be monitored regulary.

Note: Most patients should be sent to hospital to ascertain clinical and radiological diagnosis, and to permit specific acute treatments that reduce mortality and improve functional outcome. There is now good evidence from a randomised, controlled trial that inpatient care in a geographically discrete stroke unit is superior to domiciliary or supported general medical ward care with respect to survival and disability. Patients with transient ischaemic attacks and non-disabling stroke can usually be seen as outpatients provided assessment can be conducted promptly.

References: https://jnnp.bmj.com/content/70/suppl_1/i12

4. Does alcohol has any role in his attack? 

Ans. Alcohol does not seem to have much of a role in this patient as he is only an occasional drinker consuming < 180 ml once a week. 

• Epidemiological evidence indicates that recent heavy alcohol consumption increases the risk for all major types of stroke, whereas light-to-moderate alcohol intake is associated with a decreased risk of ischemic stroke.

REFERENCES:

1. https://jnnp.bmj.com/content/70/suppl_1/i12https://pubmed.ncbi.nlm.nih.gov/9778594/

5. Does his lipid profile have any role in his attack?

Ans. Studies have demonstrated a trend toward a higher risk of stroke with lower HDL-C and support HDL-C as an important modifiable stroke risk factor. In patients with recent stroke or transient ischemic attack and no coronary heart disease, only lower baseline HDL-C predicted the risk of recurrent stroke.

• HDL has anti-atherosclerotic and anti-inflammatory properties and is an important component in Atherosclerosis.
• And as this patient had a Low LDL of 33 mg/dl, that could have been contributed as a risk factor.
• Recent evidence suggests that lower HDL-cholesterol (HDL-C) may worsen the atherosclerotic process by promoting inflammation and progression from subclinical lesion to clinical event.

                                   

Protective actions of  HDL.

REFERENCES:

1. https://pubmed.ncbi.nlm.nih.gov/21830454/#:~:text=Studies%20have%20demonstrated%20a%20trend,the%20risk%20of%20recurrent%20stroke.
2. 
   
3. 
   
4. https://www.ahajournals.org/doi/10.1161/01.str.0000258347.19449.0f

   Case 2

   https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

   
   

   Complete details regarding the case are in the mentioned link above.

   
   

   ANSWERS TO CASE 2

   1)What is myelopathy hand ?

   
   

   Ans. As this patient has C3 - C6 OPLL which causes narrowing of the spinal canal and compression of the cervical spinal cord. The following sign could be observed:

   •  A characteristic dysfunction of the hand has been observed in various cervical spinal disorders when there is involvement of the spinal cord. 
   • There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers.
   • These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement. 
   • The characteristic nature of the sign permits the distinction between myelopathy and changes due to nerve root or peripheral nerve disorder. 
   • Both uncoordinated finger motion and trick motion of the wrist were more frequent in myelopathy patients than in healthy controls and uncoordinated finger motion was associated with severity of myelopathy

   
   

   REFERENCES:

   1. https://pubmed.ncbi.nlm.nih.gov/3818752/
   2. https://pubmed.ncbi.nlm.nih.gov/20354474/

   
   

   2)What is finger escape ?

   
   

   Ans. The finger-escape sign : lack of adduction and extension of the ulnar fingers.

   
   

   Grading of the finger-escape sign:

    

   Grade     Fingers                                 Deficiency

    0              All                                             None 

    1         Little finger                       Unable to hold adduction

    2         Little or little and ring       Unable to assume adduction 

    3         Little and ring                    Unable to assume adduction or full extension

    4         Little, ring and middle       Unable to assume adduction or 

   
   

   The following is a link to a video eliciting this sign:

   https://vimeo.com/517686531

   
   

   REFERENCE:

   • https://www.google.com/urlsa=t&source=web&rct=j&url=https://online.boneandjoint.org.uk/doi/pdf/10.1302/0301620X.69B2.3818752%3Fdownload%3Dtrue&ved=2ahUKEwiLypz8pe7wAhWg63MBHUvxA7cQFjAeegQILBAC&usg=AOvVaw004CpAZOiWDmjjrsAr7HgC

   
   

   
   

   3)What is Hoffman’s reflex?

   
   

   Ans. The Hoffman sign is an involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down. 

   • The reflexive pathway causes the thumb to flex and adduct quickly. 
   • A positive Hoffman sign indicates an upper motor neuron lesion and corticospinal pathway dysfunction likely due to cervical cord compression. 

   The following is a link to a video eliciting this sign:

   https://www.physio-pedia.com/Hoffmann%27s_Sign

   
   
   REFERENCE: 
   1. https://www.ncbi.nlm.nih.gov/books/NBK545156/#:~:text=%5B1%5D%20The%20Hoffman%20sign%20is,to%20flex%20and%20adduct%20quickly.
   
   
   
   
   
   

   Case 3

   https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1                

   
   

   Complete details regarding the case are in the mentioned link above.

   
   

   ANSWERS TO CASE 3

   
   

   1 What can be the cause of her condition ?

   
   

   Ans. The patient had CVT - Cortical Venous Thrombosis which occurs when a blood clot forms in the brain’s venous sinuses in smaller feeding cortical veins (cortical vein thrombosis). This  prevents blood from draining out of the brain. As a result, blood cells may break and leak blood into the brain tissues, forming a hemorrhage.

   
   

   This patient has microcytic hypochromic anemia - Fe deficiency Anemia with her HB levels falling to even 7.7 g/dl during her hospital stay.

   
   

   This could possible be the primary etiology leading to her condition due to the following reasons:

   • Serum iron is an important regulator of thrombopoiesis. Normal iron levels are required to prevent thrombocytosis by acting as an inhibitor. 
   • Iron deficiency can increase the number of platelets in blood, which is linked with a Hypercoagulable state. 
   • Erythropoietin which stimulates megakaryocytes is also increased during the iron deficiency.
   • It has been found that microcytosis decreases the cell deformability and increase the viscosity, causing abnormal flow patterns.
   • Under conditions of stress or infections, the metabolic demand at the tissue level rises which can create anemic hypoxia and can predispose to venous thrombosis.

   REFERENCE: 

   1. https://www.hopkinsmedicine.org/health/conditions-and-diseases/cerebral-venous-sinus-thrombosis
   2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401649/#:~:text=Iron%20deficiency%20anemia%20is%20a,thrombosis%20associated%20with%20minor%20infection.

   
   

   2. What are the risk factors for cortical vein thrombosis?

   
   

   Ans. Possible risk factors in this 17 year old could be:

   • Iron deficiency Anemia- Microcytic Hypochromic Anemia with HB levels falling even to 7.7 g/dl.
   • Gender predisposition ( 3:1 )
   • Pallor, Febrile temperature - mild infection?
   • Low Random blood sugars - 75 mg/dl
   • Dehydration due to vomiting episodes?
   • High PT, APTT, elevated liver enzymes - defective liver function secondary to infection/disease??

   Note: No other predisposing factors for CVT were present like sepsis, trauma, autoimmune diseases or prothrombotic disorders.

   REFERENCE:

   1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057707/
   2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3401649/#:~:text=Iron%20deficiency%20anemia%20is%20a,thrombosis%20associated%20with%20minor%20infection.

   
   

   3.There was a seizure free period in between but again sudden episode of GTCS. Why? 

   Resolved spontaneously why? 

   
   

   Ans. Levipil is an anti epileptic drug used to treat epilepsy seizures (fits). It works to avoid seizure as long as the patient keeps taking it. 

   • Levipil 500 table works by reducing irregular brain activity.
   • After the STAT I.V administration, there was a seizure free period due to the action of the drug and as soon as the drug action was worn out, there were episodes of GTCS.
   • Then the doctor administered, Inj. Phenobarbitone which decreased the brain activity and resolved the seizure. 

4. Which drug was used in suspicion of cortical venous sinus thrombosis?

Ans. Clexane 0.4 ml/SC was administered in suspicion of CVT.

• Composition - Enoxaparin Sodium
• Class of Drugs - Low Molecular weight Heparin
• Type of Drug - Anticoagulant
• Mechanism Of Action -  Binds to and potentiates Antithrombim (a circulating anticoagulant) to form a complex that irreversibly inactivates Clotting Factor Xa.
• Indication - Main treatment of acute venous sinus thrombosis to prevent propagation of the thrombus, pulmonary embolism, and decrease the risk of death or dependency even if there is intracerebral hemorrhage (ICH).

REFERENCE:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057707/

Case 4

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 4

1. What could have been the reason for this patient to develop ataxia in the past 1 year?

Ans. The causes of acquired ataxia in this patient could be:

• His Chronic alcohol consumption for the past 3 years.

1. Very common cause of Cerebella ataxia, affecting the gait and lower limbs more often.
2. The alteration in GABAA receptor-dependent neurotransmission is a potential mechanism for ethanol-induced cerebellar dysfunction.
3. Ethanol is shown to disrupt the molecular events at the mossy fiber – granule cell – Golgi cell (MGG) synaptic site and granule cell parallel fibers – PCs (GPP) synaptic site, which may be responsible for ethanol-induced cerebellar ataxia
4. Molecular events at the MGG and GPP synaptic sites are mutually reinforcing and decreases excitatory output of deep cerebellar nuclei.

• His h/o multiple falls while inebriated.

1. Concussion post fall and change in gait?

• His h/o unattended head injuries.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4492805/

2. What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

Ans. Due to Acute cerebral hemorrhage in the frontal, parietal, temporal lobe- which is an extra-axial lesion and has the potential to exert mass effect on the brain parenchyma and has caused 13mm shift of midline structures.

Chronic, heavy alcohol ingestion evidently exerts an inhibitory effect on platelet function even in the absence of alcohol in the blood. The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1341444/#:~:text=The%20impaired%20platelet%20function%2C%20together,associated%20with%20excessive%20alcohol%20intake.

Case 5

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 5

1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

Ans. This patient had gliosis which was observed on CT scan. 

The glial scar consists predominately of reactive astrocytes, microglia and extracellular matrix molecules. Astrocytes become hypertrophic, elongate their processes from the penumbra into the infarct core after ischemic stroke, and strongly up-regulate GFAP, a hallmark of astro-gliosis responding to the injury.

1. Early post stroke seizures, occur within 1 or 2 weeks of stroke and are thought to result from following cellular biochemical dysfunction leading to electrically irritable tissue such as:

• Acute ischemia leads to increased extracellular concentrations of glutamate, an excitatory neurotransmitter that has been associated with secondary neuronal injury.
• Recurrent epileptiform-type neuronal discharges can occur in neural networks of surviving neurons exposed to glutamate.
• The disturbance of electrolyte balance, the destruction of phospholipid membranes and the secretion of free fatty acids
• Calcium ion accumulation in hippocampal neurons has been known as a major contributor to the etiology of epilepsy.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3936028/
2. https://www.ahajournals.org/doi/full/10.1161/01.str.0000130989.17100.96
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5771387/#__sec11title

2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

Ans. This is a case of Simple Partial Seizure with Secondary Generalization.

Wherein, The Focal Seizure evolved into a GTCS.

• Partial seizure refers to abnormal neural activity localized to one area of the cerebral hemisphere and having a discernible focal or localized onset. 
• When there is no associated impairment in consciousness, it is called simple partial seizure, and when it is associated with impairment in consciousness, it is called a complex partial seizure.
• When a partial seizure becomes generalized, it is referred to as a "partial seizure with secondary generalization."

Triggering risk factors in this patient could be : Hypertension, Alcohol intake, Traumatic injury.

REFERENCES:

1. https://www.ncbi.nlm.nih.gov/books/NBK500005/

Case 6

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 6

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans. The evolution of the symptomatology is as follows:

7 Days back - Giddiness

- sudden onset, with 1 episode of vomiting

⬇️

Asymptomatic for 3 days and then consumed alcohol

⬇️

Giddiness

- sudden onset, gradually progressive

- Associated with aural fullness, bilateral hearing loss, tinnitus

- Increase with walking and when getting up from bed

⬇️

Vomiting 2-3 episodes/day

- Non projectile, non bilious

⬇️

H/O position instability with swaying

⬇️

2 Days ago - Slurring of speech

- Lasted 1 Day and resolved same day

⬇️

Since 2 Days - Deviation of mouth

- Lasted 1 Day and resolved same day

Patient has h/o De-novo Hypertension and irregularly following medication for it

Anatomical location:

Based on the CT scan, Cerebellar Infarct was revealed in: Right Inferior Cerebellar Hemisphere

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. De-novo Hypertension - High Blood pressure

2. Chronic Smoking - 1 pack beedi/day 

3. Chronic Alcohol consumption -  90-180 ml since past 30 years.

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans. The following interventions were used:

1. Tab Veratin 8 mg PO TID

• Meclizine, First generation antihistamine.
• Non selective H1 Antagonist with central anticholinergic effects.
• Indicated in patient's giddiness and vestibular dysfunction symptoms.
• In a double-blind crossover study, meclizine hydrochloride was shown to be significantly more effective than placebo in treating patients with positional and continuous vertigo of vestibular origin. Meclizine reduced the severity and frequency of attacks, as well as signs and symptoms associated with the vertigo. These included nausea, positional and positioning nystagmus, and postural instability.

REFERENCE: https://jamanetwork.com/journals/jamaneurology/articleabstract/571539#:~:text=In%20a%20double%2Dblind%20crossover,symptoms%20associated%20with%20the%20vertigo.

2. Inj Zofer 4 mg IV/TID

• Ondansetron, Antiemetic, 5-HT3 Antagonist.
• Indicated for patient's nausea and vomiting.
• Nausea was significantly less in the ondansetron group within the expected duration of action of a single dose of the drug (1 hr post-anesthesia) compared to placebo.

REFERENCE: https://journals.lww.com/anesthesiaanalgesia/fulltext/1998/02001/ondansetron_vs_placebo__double_blind,_randomized.342.aspx

3. Tab Ecosprin 75 mg PO/OD

• Aspirin
• Thins the blood and thereby prevents clots, is currently used to reduce the long-term risks of a second stroke in patients who've had an ischemic stroke.
• Aspirin slows the blood's clotting action by reducing the clumping of platelets. Platelets are cells that clump together and help to form blood clots. Aspirin keeps platelets from clumping together, thus helping to prevent or reduce blood clots.

REFERENCES:

1. https://www.webmd.com/stroke/news/20000601/aspirin-after-stroke-helps-prevent-another
2.  https://www.uofmhealth.org/health-library/te7903spec

4. Tab Atorvostatin 40 mg PO/HS

• Statins lower serum cholesterol level by inhibiting hydroxymethylglutaryl-coenzymeA (HMG-CoA) reductase.
• The beneficial effect of statin therapy on the risk of recurrent stroke was due to a reduction in the risk of cerebral infarction, the mechanism of which largely has been attributed to a reduction in LDL cholesterol levels. The lower average LDL cholesterol level achieved in the atorvastatin as compared with the placebo group is consistent with this hypothesis.
• Decreased the risk of stroke, major coronary events, and revascularization procedures. These results support the initiation of atorvastatin treatment soon after a stroke or TIA.

REFERENCES:

1. https://www.nejm.org/doi/10.1056/NEJMoa061894#:~:text=In%20conclusion%2C%20in%20patients%20with,after%20a%20stroke%20or%20TIA.
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428028/

5. BP monitoring- 4rth hourly

6. Tab Clopidogrel 75 mg PO/OD

• Antiplatelet drug
• Clopidogrel blocks platelet aggregation through the P2Y 12 -receptor pathway, a mechanism that is synergistic with aspirin in platelet-aggregation assays.
• Combination antiplatelet therapy with clopidogrel and aspirin may reduce the rate of recurrent stroke during the first 3 months after a minor ischemic stroke or transient ischemic attack (TIA). A trial of combination antiplatelet therapy in a Chinese population has shown a reduction in the risk of recurrent stroke.

REFERENCE: https://www.nejm.org/doi/full/10.1056/nejmoa1800410#:~:text=Combination%20antiplatelet%20therapy%20with%20clopidogrel,the%20risk%20of%20recurrent%20stroke.

7. Inj Thiamine 1 AMP in 100 ml NSPO/BD

• Vitamin B1 supplementation.
• Necrotic cell death after cerebral ischemia triggers the activation of the immune system, followed by an inflammatory response. It is likely that fatigue related to stroke could benefit from high-dose thiamine. 

REFERENCE: https://pubmed.ncbi.nlm.nih.gov/25192035/#:~:text=Necrotic%20cell%20death%20after%20cerebral,or%20parenteral%20high%2Ddose%20thiamine.

8. Tab MVT PO/OD

• MethylCobalamin, Viatmin B12 supplementation.
• Mecobalamin can reduce the level of plasma homocysteine, then lead to reductions of levels of plasma inflammatory factors and volume of carotid artery plaques, resulting in more significant functional recovery.

REFERENCE: https://www.scielo.br/j/ramb/a/B6ZMVDg3wpZbwJJjg3g9SHk/lang=en#:~:text=For%20patients%20with%20H%2Dtype,improve%20the%20prognosis%20of%20patients.

3. Did the patients history of denovo HTN contribute to his current condition?

Ans. The patient's hypertension could have aided in causing the stroke in the following ways:

• A high intraluminal pressure will lead to extensive alteration in endothelium and smooth muscle function in intracerebral arteries. 
• The increased stress on the endothelium can increase permeability over the blood-brain barrier and cause local or multifocal brain edema.
• Endothelial damage and altered blood cell-endothelium interaction can lead to local thrombi formation and ischemic lesions. 
• Fibrinoid necrosis can cause lacunar infarcts through focal stenosis and occlusions.
• Degenerative changes in smooth muscle cells and endothelium predisposes for intracerebral hemorrhages. 
• Furthermore, hypertension accelerates the arteriosclerotic process, thus increasing the likelihood for cerebral lesions related to stenosis and embolism originating from large extracranial vessels, the aortic arch and from the heart. 
• Adaptive structural changes in the resistance vessels, while having the positive effect of reducing the vessel wall tension, have the negative consequence of increased peripheral vascular resistance that may compromise the collateral circulation

REFERENCE:

1. https://pubmed.ncbi.nlm.nih.gov/10405790/#:~:text=Hypertension%20can%20cause%20stroke%20through,local%20or%20multifocal%20brain%20oedema.

4. Does the patient's history of alcoholism make him more susceptible to ischemic or hemorrhagic type of stroke?

Ans. As the patient had cerebral infarction, it is most likely ischemic stroke and due to the chronic high intakes of alcohol, following acute potentially deleterious physiologic effects within hours after consumption can develop, including:

• Impaired fibrinolysis.
• Alcohol induced vasoconstriction.
• Increased platelet activation.
• Hyper homo-cysteinemia.
• Increased blood pressure and heart rate. 
• Heavy consumption may acutely lead to dehydration, further increasing the transient risk of stroke.

 REFERENCES: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937356/

Case 7

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 7

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans. The evolution of the symptomatology is as follows:

H/O seizure episode 1 year back

⬇️

4 Months ago - Another episode of Seizure

- Mostly post alcohol cessation

- Sweating/Restlessness/Tremors

⬇️

9 Days back - Talking and laughing with himself

- sudden onset

- unable to move around or lift himself off the bed

⬇️

Since 9 Days - Decreased food intake

⬇️

Since 9 Days - Short Term Memory Loss

Patient is k/c/o Type 2 Diabetes Mellitus since 2 years and is irregularly following medication for it.

Patient also has a h/o chronic smoking and alcohol since 12 years.

Anatomical location:

Based on the patient's history, Wernicke's Encephalopathy was revealed hence: periventricular region, diencephalon, the midbrain, hypothalamus, and cerebellar vermis.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Type 2 Diabetes Mellitus

2. Chronic Smoking - 10 cigarettes/day 

3. Chronic Alcohol consumption -  3-4 quarters/day since past 12 years.

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans. 

1. IVF NS and RL @150ml/hr

• To prevent dehydration, maintain fluid volume.

2. Inj. 1amp THIAMINE in 100ml NS, TID

• Thiamine ( B1 ) is the primary treatment in Wernicke's encephalopathy.

3. Inj. Lorazepam

• Short Acting Benzodiazepine for treating the patient's chronic alcoholism withdrawal symptoms.
• REFERENCE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606320/

4. T. Pregabalin 75mg/PO/ BD

• Anticonvulsant, anxiolytic for alcohol withdrawal symptoms
• Good efficacy, safer drug.
• REFERENCE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5124051/

5. Inj. HAI S.C.- premeal

• To keep the elevated sugar levels under check, patient is a k/c/o DM type 2.

6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am

• To check for any signs of uncontrolled sugars, to avoid complications.

7. Lactulose 30ml/PO/BD

• To prevent complications of hepatic encephalopathy

8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours

• To combat lose of potassium and chloride ions in urine due to alcohol intake, kidney injury.

9. Syp Potchlor 10ml in one glass water/PO/BD

• For low levels of potassium.

3. Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

Ans. Alcohol increases the effects of GABA, a neurotransmitter responsible for creating feelings of calm and euphoria. It also decreases Glutamate, another neurotransmitter that creates excitability.

• Heavy drinking makes it harder and harder to increase GABA and decrease glutamate, so more and more alcohol is required for the same outcome. Your body becomes accustomed to these changes and responds by producing more glutamate and less GABA.

• When you suddenly stop drinking, you are no longer impacting these two neurotransmitters, but your body is still over producing glutamate and underproducing GABA. 

• As a result, you may become hyper excited: anxious, restless, and shaky. If you were a heavy drinker, your symptoms may be much more severe, progressing to tremors, seizures, and serious high blood pressure.

4. What is the reason for giving thiamine in this patient?

Ans. Wernicke’s encephalopathy is an acute neuropsychiatric disorder that occurs as a result of thiamine (vitamin B1) deficiency. 

• As thiamine blood levels fall, thiamine-dependent enzyme systems involved in prevention of cellular damage become impaired and metabolic demands increase, which can result in selective brain lesions correlated with Wernicke’s encephalopathy.
• Consequently, thiamine deficiency and development of WKS is particularly prevalent in malnourished patients oftentimes due to the shift in diet away from vitamin-rich foods and, as in the case of chronic alcoholism, a shift towards the carbohydrate-heavy consumption of alcohol.

Thiamine replacement is the primary treatment in order to reverse mental status changes and prevent further disease progression. Parenteral thiamine is used in the acute treatment of Wernicke’s since intestinal absorption of thiamine may be impaired, as in the case of alcoholics

REFERENCE: 

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354137/#:~:text=Wernicke's%20encephalopathy%20is%20an%20acute,nystagmus%20and%20ophthalmoplegia%20(1).

5. What is the probable reason for kidney injury in this patient? 

Ans. The patient was a chronic alcoholic since 12 years hence, oxidative stress resulting from increased production of reactive oxygen species, which leads to an excessive amount of free radicals, Ischemia and dehydration which in turn trigger tissue injury and increase inflammation is a common possible mechanism.

Possible mechanism for alcohol-induced kidney injury. 

Chronic alcohol consumption induces profound injury in several organs that may affect and aggravate the deleterious effect of ethanol on the kidney. 

• Ethanol itself markedly induces the expression of the microsomal ethanol oxidation system (CYP2E1), producing reactive oxygen species as a byproduct. 
• Increased gastrointestinal permeability and endotoxin load may lead to alcoholic steatohepatitis resulting in excessive immunoglobulin A (IgA) load (due to increased intestinal production and decreased hepatic IgA clearance). 
• IgA deposits may accumulate in the kidney, leading to glomerulopathy. Renal microcirculatory alterations in advanced liver cirrhosis leads to hepatorenal syndrome. 
• Alcohol-induced skeletal muscle damage leads to excessive amounts of circulating myoglobin, causing renal tubular injury as a result of increased oxidative stress. Due to the development of alcoholic cardiomyopathy, chronic renal hypoxia develops, activating the renin–angiotensin–aldosterone system (RAAS), which in turn leads to further free radical production and to the propagation of fibrotic pathways.

REFERENCE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5513691/

6. What is the probable cause for the normocytic anemia?

Ans. Most of the normochromic, normocytic anemias are a consequence of other diseases.

1. Increase in pro-inflammatory cytokines and iron dysregulation - Alcohol, Diabetes, Smoking, poor nutrition, malabsorption.
2. Inappropriate erythropoietin (EPO) levels or less response to erythropoietin - Alcohol effects on Bone marrow, kidney dysfunction.
3. Decreased RBC survival and Bone Marrow Infiltration - Bone marrow toxicity due to alcohol dependence and smoking.

REFERENCES: https://www.ncbi.nlm.nih.gov/books/NBK565880/

7. Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

Ans. This patient has 3 major chronic issues - CHRONIC SMOKING, CHRONIC ALCOHOLIC and DIABETES MELLITUS TYPE 2.

Now in such patients there are various factors which aggravate foot ulcers and delay their healing:

• Poor blood flow in the extremities.
• Peripheral Arterial disease, Peripheral Neuropathy
• Decreased tissue perfusion and oxygenation due to toxic by products such as carbon monoxide, hydrogen cyanide, etc.
• Nicotine - Affects osteoblasts and delays bone healing, decreased tissue perfusion.
• Poor nutrition impairs wound healing.
• Ethanol exposure can lead to impaired wound healing by impairing the early inflammatory response, inhibiting wound closure, angiogenesis, and collagen production, and altering the protease balance at the wound site.

REFERENCES:

1. https://www.researchgate.net/publication/301827503_A_study_on_the_impact_of_smoking_and_alcoholism_as_determinant_factors_in_the_prognosis_and_outcome_of_diabetic_foot_ulcer_disease
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903966/#:~:text=In%20summary%2C%20acute%20ethanol%20exposure,balance%20at%20the%20wound%20site.

Case 8

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 8

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans. The evolution of the symptomatology is as follows: 

8 Months ago - Bilateral Pedal Edema

- Gradual, Pitting type

⬇️

2 Months ago - Neck pain

- Medication given

⬇️

Since 6 Days - Radiating Pain along Left Upper limb

- Dragging in nature, associated with Numbness and Tingling sensation

- Aggravated with Palpitations and relieved on medication

⬇️

Since 5 Days - Palpitations

- Sudden onset, more in the nights

- Aggravated by lifting weights, speaking continuously 

- Relived by Drinking water and on medication

⬇️

Since 5 Days -  Chest pain with Chest heaviness

⬇️

Since 5 Days - Dyspnea (NYHA class 3)

- Generalized body weakness

Patient has h/o paralysis of all 4 limbs 10 years back.

                   h/o paresis on both sides due to hypokalemia 1 year back.

                  h/o blood infection 7 months back.

Anatomical location:

Based on the history - Radiating Pain along Upper limb - compression of nerve root near cervical vertebrae (radiculopathy) due to cervical spondylosis.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Hypokalemia causing - Palpitations, Chest Heaviness, Generalized weakness, Dyspnea, Limbs numbness. 

2. Raised ESR of 100mm/1st hour - Infection or Inflammation

3. Her Cervical spondylosis causing Tingling sensation in limbs.

4. Psychogenic/Anxiety/ stress - Palpitations, Difficulty in breathing. 

2. What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

Ans. Reason for recurrence could be: DIURETICS administration leading to excess loss of potassium in urine.

Risk Factors: 

• Diuretic Therapy
• Female gender
• Alcohol Intake
• Inadequate intake - anorexia, malnutrition, starvation
• Diarrhea, Excess vomiting
• Hypertension
• Heart failure
• Alkalosis, Mi, Head injury
• Cushing's Syndrome
• Respiratory Alkalosis
• Cystic fibrosis
• Excessive sweating
• Severe Burns
• Transcellular shifts - Diabetic Ketoacidosis

3. What are the changes seen in ECG in case of hypokalemia and associated symptoms?

Ans.               Normal ECG:

  

1. 1. Changes in ECG in Hypokalemia:
      1. T – waves are depressed.
      2. P – wave has peaked.
      3. ST – depression.
      4. U- wave is prominent.

Signs And Symptoms

1. Potassium level < 2.5 meq/L 
   1. There will be tachycardia.
   2. There is increased muscular irritability.
      • There are specific cardiac conduction defects.
      • There is stoppage of the heart in the systole.
   3. There is a flattened T – wave.
   4. The end result will be cardiac arrest.
2. Potassium level <3.0 meq/L - There are marked neuromuscular symptoms.

REFERENCE: https://www.labpedia.net/electrolytes-part-1potassium-k-blood

INFECTIOUS DISEASES

Case 1

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

Complete details regarding the case are in the mentioned link above.

ANSWERS TO CASE 1

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans. The evolution of the symptomatology is as follows: 

3 Years ago - Hypertension diagnosed

⬇️

Since 10 Days - Fever

⬇️

Since 4 Days  - Facial Puffiness and Periorbital edema

⬇️

Since 4 Days - Weakness of both upper and lower limbs of right side

⬇️

Since 2 Days - Altered sensorium, irritable

patient also complained of fever with chills and rigor post-covid Vaccination.

Diabetic Ketoacidosis, Denovo Diabetes type 2 and CKD was diagnosed during the hospital stay.

Anatomical location:

As the patient has Acute Oro-Rhino-Orbital Mucormycosis, the site of abnormality is:

• Medial canthus, eyelids, periorbital area
• Hard palate
• Sinuses, Left nasal cavity

Patient also has Right sided CVA, the site of abnormality is - Left frontal and temporal lobe.

Primary Etiology:

Based on the patients history, primary etiological factors could be:-

1. Diabetic Ketoacidosis - Immunocompromised

2. Post COVID Vaccination

2. What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would you approach this patient as a treating physician?

Ans. Drugs used are as follows:

1. Inj. Liposomal Amphotericin B 

• Lipid formulations of amphotericin B (LFAB) have evolved as the cornerstone of primary therapy for Mucormycosis. 
• LFABs appear to be less nephrotoxic, safer, efficacious alternatives to AmB for the treatment of Mucormycosis. 
• Better CNS penetration than AmB and improved outcomes vs. AmB in murine models and a retrospective clinical review. 

2. 200mg of itraconazole
3. Deoxycholate amphotericin B (AmB)

• >5 Decades clinical experience.
• Inexpensive.
• Only licensed agent by US Food and Drug Administration for the treatment of Mucormycosis.

REFERENCE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2809216/

Approach as follows: The therapeutic approach to Mucormycosis is multimodal:

 Early Diagnosis.

Antifungal Agents.

 Surgical Debridement.

 Correction & Control of Underlying Predisposing Condition.

 Rapid correction of metabolic abnormalities - mandatory in uncontrolled diabetes.

 Corticosteroids should be discontinued, if feasible.

Other Immunosuppressive drugs should be tapered as much as possible.

REFERENCE: https://www.haematologica.org/article/view/6614

3. What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?

Ans.  As of May 22, the government has reported 8,848 cases of this fungal disease, which can lead to serious complications and has a high rate of mortality

The postulated reasons for this rise of cases could be:

• Improper use of steroids - too early, excess dose, prolonged period.

 "In India, the problem lies not in the drug but in how it is prescribed."

• Poor Management of Diabetes.
• Late diagnosis of Diabetes.
• Over diagnosis and over treatment. 

"For instance, a zinc supplement is commonly prescribed to Covid-19 patients at high doses, supposedly to increase immunity and aid the body in fighting the virus. Pinto and others like Rajeev Jayadevan, consultant gastroenterologist at Kochi’s Sunrise Group of Hospitals, have been particularly concerned about the possible role of zinc in aiding the fungal infection to take root."

• Lack of a strict prescription check.
• Improper use of oxygen cylinders - outdated tanks, unclean masks and unpurified water in the apparatus.

REFERENCE:

1.  https://qz.com/india/2012257/why-india-has-so-many-cases-of-mucormycosis-or-black-fungus/

COVID CASES

The following is the link to a master chart on the compiled COVID cases for May 2021:

https://docs.google.com/spreadsheets/d/1WcvDUej1Rpsfa-4zo1dguZX8YD543NuySO6s0t-lEXU/edit?usp=sharing

REFLECTIVE LOGGING OF THE EXPERIENCE

This experience of an online tele medical log book wherein we have analyzed, researched and learned about various cases has been extremely enriching clinically.

While maintaining these E-logs, we have tried to understand the core system of each of our assigned case, correlated it to the other systems, interlinked the basic sciences and learnt about the basic approach to a patient including the various treatment modalities. Each case had a set of intriguing questions framed by my peers which has only made this entire experience more challenging and wholesome.

Due to the pandemic, we got more time to carefully review each clinical scenario and in understanding the methodology of approaching a patient in a clinical setting. Though the ideal way of learning would be by physically interacting with the patient and learning by doing, for these unprecedent times, this mode of learning is our best and most effective option. 

For that I would like to thank Dr. Rakesh Biswas, HOD, General Medicine for his guidance and this opportunity and actively including us in all portals of clinical discussion.

I would also like to thank all the interns, post graduates and professors of General Medicine department for taking the time out for providing us with all the necessary data.