Blended Assignment for the month of May, 2021

I have been given the following cases to solve in an attempt to understand Patient clinical data analysis, and to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations, and diagnosis- in order to formulate a strong treatment plan.

This is the link to the questions asked:

http://medicinedepartment.blogspot.com/2020/09/medicine-paper-for-october-2020-first.html?m=1

Below are the answers based on my comprehension of the cases: 

PULMONOLOGY

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

QUESTIONS:

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?

Symptomatology:

20 years ago: she had an episode of SOB (grade II) during the month of January while working on the paddy fields. Decreased on taking inhalers. Repeated every year.

                                        🠟                                        

12 years ago: she had a severe episode of SOB that required hospitalization after which her symptoms reduced.

🠟

8 years ago: she was diagnosed with diabetes

🠟

5 years ago: treated for anemia with iron injections 

🠟

1 month ago: she was experiencing generalized weakness 

🠟

30 days ago: had her latest episode of SOB

🠟

20 days ago: had an HRCT done due to suspicion of COVID

🠟

15 days ago: developed pedal edema

🠟

15 days ago: developed facial puffiness 

🠟

2 days ago: reduced urine output 

Anatomical localization: Lungs

Etiology: COPD that lead to her right heart failure. The COPD is probably a consequence of using a indoor stove (choolha)

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

1. Augumentin

• MOA: Amoxicillin is a beta lactam antibiotic that acts by preventing the cross linking of bacterial cell wall. Clavulanic acid acts by protecting Amoxicillin from being inactivated by beta lactamases.

• Indication: lower respiratory tract infections, otitis media, skin infections, UTI, sinusitis, etc

• Efficacy: highly effective against sensitive strains of: staphylococci, E. Coli, klebsiella, Proteus as compared to placebo or ampicillin.

2. Azithromycin:

• MOA: prevents bacterial protein synthesis by preventing the translocation step by binding to 50s subunit.

• Indication: Community acquired pneumonia, tonsillitis, acute exacerbation of COPD, PID

• Efficacy: effective against staphylococci, streptococcus and moroxella along with many other gram positive and negative bacteria

3. Lasik

• MOA:  it is furosemide that is a loop diuretic that acts by blocking the Na+k+cl- transport channel in the loop of Henle

• Indications: heart failure, liver cirrhosis, kidney disease

• Efficacy: highly effective diuretic

4.Pantop

• MOA: it is a proton pump blocker that decreases gastric acid secretion

• Indications: acidity

• Efficacy: highly effective

5.Hydrocortisone

• MOA: it is a steroid drug that decreases inflammation

• Indication: asthama, COPD, thyroiditis,Rheumatoid arthritis, adrenocortical insufficiency

• Efficacy: highly effective

6. Ipravent

• MOA: An anti cholinergic that causes bronchodilation

• Indications: bronchial asthama , COPD

• Efficacy: highly effective

7. Budecort

• MOA;beta 2 agonist that causes bronchodilation.

• Indications: asthama, COPD, COVID

• Efficacy: highly effective

8. Pulmoclear

• MOA: acebrophylline:acts by bronchodilation, anti inflammatory action and as a mucolytic.                    Acetylcysteine: has mucolytic action.

• Indications: COPD

• Efficacy: highly effective

9. Thiamine

• MOA: thiamine diphosphate is a coenzyme in carbohydrate metabolism

• Indications: deficiency, wernicke's encephalopathy, beriberi

10. O2 supplementation

• MOA: Acts by increasing alveolar oxygen partial pressure

• Indications: decreased SPO2

11.Chest physiotherapy

• MOA: expands lungs' strengthen s respiratory muscles, improves drainage of mucus.

• Indications: COPD, bronchiectasis, cystic fibrosis

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

The causes for acute exacerbation of COPD could include:

• Respiratory infections: responsible for half of all acute exacerbations. Commonly due to H. Influenzae, S. Pneumoniae, Moraxella catarrhalis.

• Allergens: like pollen, wood smoke

• Air pollution 

• Toxins

4) Could the ATT have affected her symptoms? If so how?

• It's possible that the ATT resulted in Acute Kidney Injury.
• According to the history the patient started developing pedal edema and facial puffiness a few days after starting on ATT. 
• As facial puffiness and pedal edema are both signs of renal dysfunction it is possible that some of her symptoms are due AKI as a consequence of adverse reaction to ATT.

5) What could be the causes for her electrolyte imbalance?

•  The patient has hyponatremia and hypochloremia.
•  The hyponatremia can be a consequence of AKI. In AKI there is a loss of renal function compromising its ability to reabsorb sodium leading to excess urinary sodium loss. Hence the hyponatremia.
• The patient is also suffering from hypochloremia which could be a consequence of her heart failure in addition to her treatment with diuretics such as lasix (furosemide).  

2) NEUROLOGY

CASE 2a:

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

Questions: 

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?

Symptomatology:

                                  2009 (12 years ago): Started drinking alcohol

                                                                     🠟

       2019 (2 years ago): Diagnosed with Diabetes Mellitus, prescribed oral hypoglycemics

                                                                     🠟 

                 2020 (1 year ago): Has an episode of seizures (most likely GTCS)

                                                                     🠟                                                 

January 2021 (4months ago): Has another seizure episode (most likely GTCS)- following cessation of alcohol for 24 hours. Starts drinking again after the seizure subsides

                                                                     🠟

Monday, May 10, 2021: Last alcohol intake, around 1 bottle. Starts having general body pains at night.

                                                                     🠟

Tuesday, May 11, 2021: Decreased food intake. Starts talking and laughing to himself. Unable to lift himself off the bed, help required. 

                        Conscious, but non-coherent. Disoriented to time, person, place.

                                                                     🠟

                  Goes to an RMP the same day- is prescribed IV fluids and asked to visit a hospital

                                                                     🠟   

Saturday, May 15, 2021: Is admitted to a tertiary care hospital for alcohol withdrawal symptoms, and is treated for the same.

Anatomical localization: The most probable location in the brain is the hippocampus and frontal lobe.

Etiology: Chronic Alcoholism with repeated withdrawal

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

1. IVF NS and RL @150ml/hr

MOA: 

 Indication: For dehydration

Efficacy: Highly effective, for severe dehydration

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

MOA: Thiamine is necessary to provide energy to the CNS, helps in the conduction of nerve signals.

Hence, deficiency leads to confusion and ataxia, both of which are present in this patient.

Indication: Since Wernicke syndrome (deficiency of B1 vitamin) is a differential diagnosis.

Efficacy: Highly effective in treating B1 deficiency

3. Inj. Lorazepam

MOA: increases chloride channel opening, facilitates GABA release

 Indication: Used to sedate patient

Efficacy: High efficacy

4. T. Pregabalin 75mg/PO/ BD

MOA: Acts by releasing GABA

Indications: in seizures

Efficacy: Newer antiepileptic, good efficacy with fewer side effects

5. Inj. HAI S.C.- premeal

MOA: Short-acting insulin

Indications: Diabetes Mellitus

Efficacy: Effective for short periods of time

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

7. Lactulose 30ml/PO/BD

Given for same reason as Ringer's lactate

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

9. SypPotchlor 10ml in one glass water/PO/BD

MOA: Potassium to increase serum K levels

Indications: in hypokalemia

Efficacy: Highly effective

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

A possible cause for this is a phenomenon known as kindling. 

In kindling, repeated attempted alcohol detoxification leads to increased severity of the withdrawal syndrome. Patients with previous withdrawal symptoms are more likely to have more medically complicated withdrawal symptoms with time. 

Chronic alcohol use and kindling together lead to permanent alteration in GABA receptors, leading to downregulation of GABA. This in turn leads to inhibition of inhibitory neurotransmitter GABA, hence leading to seizures (hyperactivity).

Source: https://en.wikipedia.org/wiki/Alcohol_withdrawal_syndrome

4) What is the reason for giving thiamine to this patient?

One of the differential diagnoses for altered sensorium following chronic alcoholism is Wernicke-Korsakoff Syndrome, caused by deficiency of thiamine (B1). To either treat or rule this differential out, thiamine is given.

Thiamine is necessary to provide energy to the CNS, helps in the conduction of nerve signals.

Hence, deficiency leads to confusion and ataxia, both of which are present in this patient.

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

As the urea levels are very high, it denotes an acute onset- Acute Renal Failure.

As high serum creatinine and urea levels are present, denotes that reabsorption from tubules is taking place- therefore the primary cause is prerenal, most probably due to generalized dehydration.

A slightly high FENa level also denotes that tubular necrosis is occurring to some degree, hence the Prerenal AKI (mostly due to dehydration) is in turn leading to Acute Tubular Necrosis (ATN).

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

Possible causes:

a. Increased oxidative stress and inflammation, leading to hemolysis of the RBCs

b. Decreased bone marrow production of RBCs, due to EPO deficiency owing to kidney failure

c. Loss of blood through chronic foot ulcer

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

Yes, as alcoholism itself can cause peripheral neuropathy (alcoholic neuropathy), which along with Diabetic neuropathy, can lead to a non-healing foot ulcer.

CASE 2b: 

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

QUESTIONS:

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?

Symptomatology:

        Since 1991, 30 years ago: The patient has been drinking alcohol, 90-180ml per day

                                                                 🠟

                 May 13, 2021: Feels giddy, subsides after a while. One episode of vomiting

                                                                 🠟

                                        May 13-16: Stops consumption of alcohol

                                                                 🠟

                                        May 16, 2021: Consumes alcohol again

                                                                 🠟 

May 17, 2021: Another bout of giddiness, associated with Bilateral hearing loss, aural fullness, tinnitus, nystagmus, 2-3 episodes of vomiting per day.

                                                                 🠟

                               May 18, 2021: Admitted to a tertiary care hospital.

Anatomical location: Infarct in the right inferior cerebellar hemisphere

Etiology: Cerebellar infarction, most probable cause: Primary HTN

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

InjZofer 4 mg IV/TID

MOA: 5-HT receptor antagonist

Indication: Ondansetron, used as an antiemetic

Efficacy: Effective

Tab Ecosprin 75 mg PO/OD

MOA: Aspirin, Cyclo-oxygenase inhibitor

Indication: To prevent strokes

Efficacy: Used as a preventive measure

Tab Atorvostatin 40 mg PO/HS

MOA: Statin, HMG CoA reductase inhibitor

 

Indication: To decrease cholesterol levels

Efficacy: To prevent stroke recurrence

BP monitoring- 4rth hourly

Tab Clopidogrel 75 mg PO/OD

MOA: Inhibits activation of GP2b/3a activation, therefore prevents platelet aggregation

Indication: Antiplatelet

Efficacy: To prevent stroke recurrence

Inj Thiamine 1 AMP in 100 ml NSPO/BD

MOA: Provides Vitamin B1

Indication: In case B1 deficiency exists

Efficacy: Not effective in this case

3) Did the patient's history of denovo HTN contribute to his current condition?

• Yes, a cerebellar infarct is a type of ischaemic stroke, which occurs due to infarction following decreased blood supply to that area.
• Since HTN causes hyaline arteriosclerosis, and eventually rupture, HTN is a cause for stroke and in turn, cerebellar infarcts.

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

• Binge drinking causes hyperlipidemia with an increase in LDL, which in turn leads to atherosclerosis.
• Atherosclerosis of the vessels to the brain leads to ischemia, hence causing an ischaemic stroke.

CASE 2C:

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

QUESTIONS:

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?

Symptomatology:

2011, 10 years ago: One episode of quadriplegic paralysis

                                     🠟

October 2020: Developed bilateral pedal edema, pitting type

                                     🠟

May 10, 2021: Pain along the left upper limb, dragging in nature

                                     🠟

May 11, 2021: Palpitations, sudden in onset, associated with dyspnoea (grade 3), Chest pain with chest heaviness.

Anatomical localization: Skeletal muscle, Neuromuscular junction

Primary etiology: Hypokalemia (decreased serum potassium)

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

• Possibly inherited or idiopathic causes for hypokalemia.
• Risk factors of hypokalemia:

1. Female

2. Medications (diuretics)

3. Heart failure

4. Hypertension

5. low BMI

6. Alcoholism

7. Diarhhoea/ severe vomiting

8. Cushing syndrome

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

Changes seen include a shallow or inverted T wave, QT prolongation in mild hypokalemia, and

Visible U wave, mild ST depression in severe hypokalemia. 

CASE 2D

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

QUESTIONS:

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

Yes, there is. Post-stroke seizures occur more often after a hemorrhagic stroke and are more likely to be recurrent when they are late-onset seizures. 

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585721

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

After-effects of stroke include scar formation, leading to gliotic scarring as seen in this patient. Increased scarring may have led to worsening of symptoms, hence causing loss of consciousness in the recent episode.

CASE 2E

E) Link to patient details:

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

Questions:

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

• The patient was a chronic alcoholic who started drinking 3 years ago. He represents a classic case of cerebellar ataxia due to toxic damage by alcohol. 

Alcohol causes cerebellar ataxia by various mechanisms:

1. It is said to increase GABA release in Purkinje cells, granule cells, and molecular layer interneurons and causes Bergmann gliosis.
2. It causes dendritic regression by affecting the smooth endoplasmic reticulum of the Purkinje cell dendrites
3. It alters the functioning of other areas of the brain that receive cerebellar input by hindering the development of cerebellar circuitry after the loss of Purkinje cells

• Chronic alcohol abuse can also lead to thiamine deficiency that manifests in the form of Wernicke's encephalopathy- a triad of ataxia, ophthalmoplegia, and confusion
• Alcohol-induced cerebellar ataxia is due to the primary involvement of the anterosuperior region of the cerebellar vermis( lingula, central lobe, culmen,declive) which presents with volume loss

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

Patient factors: 

• This patient has a history of an alcohol binge a few hours prior to the onset of symptoms.
• He has a history of repeated falls and head trauma over the past 2-3 years that went undetected and were medically unattended. 
• He has no history of hypertension but was reported to be hypertensive after the development of intracranial bleeding (BP: 150/90) 

How does alcohol contribute to bleeding diathesis?

• Chronic alcoholism blunts the liver's ability to produce coagulation factors and increase fibrinolysis. Alcoholics often show abnormal prothrombin time and partial thromboplastin time due to a lower than normal platelet count, which can gradually weaken the walls of blood vessels.
• Acute intoxication with alcohol also simulates a hypertensive state that lasts while the drug is in the system, with the body returning to a normotensive state during withdrawal from alcohol.
• Cerebral hemorrhage can lead to an increased ICP that can cause subfalcine herniation( cingulate gyrus) or transtentorial herniation due to mass effect, such as the one seen in this patient. 
  
  
  

  
  
  
  
  
  

Source: https://sci-hub.se/10.1161/01.str.19.12.1565

CASE 2F

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

QUESTIONS:

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

Yes. Trauma to the head in an RTA may cause axonal shearing as well as microthrombi formation, both of which can aggravate a stroke. 

 Source: https://www.mayoclinicproceedings.org/article/S0025-6196(13)01089-6/pdf

2.What are the warning signs of CVA?

1. Sudden confusion, trouble speaking, or difficulty understanding speech.

2. Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.

3. Sudden trouble seeing in one or both eyes.

4. Sudden trouble walking, dizziness, loss of balance, or lack of coordination.

3.What is the drug rationale in CVA?

1. Mannitol, osmotic agent- to decrease cerebral edema, increase cerebral perfusion

2. Aspirin, antiplatelet- prevention of stroke again, to prevent other thrombotic events

3. Atorvastatin, to decrease LDL- prevention of another stroke

4. Does alcohol has any role in his attack?

• Alcohol causes hyperlipidemia with an increase in LDL, which in turn leads to atherosclerosis.
• Atherosclerosis of the vessels to the brain leads to ischemia, hence causing a stroke.

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

Yes, an increase in LDL with time leads to atherosclerosis. Atherosclerosis of the vessels of the brain leads to ischemia, causing a stroke.

CASE 2G

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

QUESTIONS:

1)What is myelopathy hand?

• Myelopathy hand refers to the loss of adduction and extension of the last two fingers, along with the inability to grip objects with these fingers. There is wasting of muscles present

• Pathophysiology: Due to pyramidal tract involvement. Hence, the only motor system involved, no sensory involvement.

• Seen in cervical spine disorders with spinal cord involvement.

2)What is finger escape?

• Sign of cervical myelopathy

• Procedure: Ask the patient to extend and abduct fingers. The last 2 fingers become flexed and adducted in 30 seconds due to poorly innervated interosseous muscles in cervical myelopathy.

3)What is Hoffman’s reflex?

• Refers to loosely holding the middle finger and flicking the fingernail downward, allowing the middle finger to flick upward.

• Positive: Flexion and adduction of the thumb, and flexion of the index finger.

• A positive Hoffmann's sign is suggestive of corticospinal tract dysfunction localized to the cervical segments of the spinal cord.

 

CASE 2H

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

QUESTIONS:

1) What can be the cause of her condition?               

• The patient had acute cortical vein thrombosis leading to a hemorrhagic venous infarction. 
• In cortical vein thrombosis, close contact of cortical veins to the cerebral cortex can cause local alterations of the blood-brain barrier and trigger seizures.
•  Also, the occlusion of veins that drain venous blood from the motor and sensory cortices increases the risk of seizures due to motor cortex damage.
• If hemorrhage occurs, focal cortical irritation caused by blood metabolites could also cause seizures.              
  
  
  
  
  

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

• Coagulopathies: antiphospholipid syndrome, protein C and S deficiency, AT III deficiency

• Cancer

• Pregnancy

• Obesity 

• Collagen vascular disorders 

• Intracranial hypotension.

• Inflammatory bowel diseases: Crohn's disease, ulcerative colitis.

3)There was a seizure-free period in between but again sudden episodes of GTCS why? Resolved spontaneously why?   

The seizure-free period could be because seizures after CVA are of two types: 

• Early seizures: Seen within 24 days of the incident.
  The seizure on May 1 2021 may have been an early type.
• Late seizures: Occur at least 1-2 weeks after the incident.
  The seizure on May 10, 2021, may have been late type.                        

             

4) What drug was used in suspicion of cortical venous sinus thrombosis?

Clexane (enoxaparin)- anticoagulant

Mannitol- osmotic agent, to decrease intracerebral pressure 

CARDIOLOGY

CASE 3A

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

QUESTIONS:

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

1) Heart failure with preserved ejection fraction AKA diastolic heart failure: 

• Preserved ejection fraction
• Normal EDV
• Decreased compliance (Increased EDP) usually secondary to myocardial hypertrophy
• Concentric LV modelling
• High LV mass
• Cardiomyocyte hypertrophy

2) Heart failure with reduced ejection fraction AKA systolic heart failure:

• Reduced EF
• Increased EDV
• Decreased contractility often secondary to ischemia/MI or dilated cardiomyopathy
• Eccentric LV modelling
• Low LV mass
• Cardiomyocyte loss

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

A possible reason for not doing pericardiocentesis could be that the patient was hemodynamically stable and his pericardial effusion was improving with the medical treatment itself. It had come down from 2.4 to 1.9cm.

             

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

Risk factors in this patient: 

• Diabetes 

• Hypertension 

• Smoking

• Alcohol consumption 

• Anemia

• Old age

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

• The patient has diastolic dysfunction, which can lead to hypovolemia, which causes hypotension. 
• The patient is also on diuretics which can also lead to hypovolemia. 
• Anemia can also be a contributing factor to hypotension.                           

CASE 3B

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

QUESTIONS:

1.What are the possible causes for heart failure in this patient?

Possible causes may be old age, anemia, diabetes, alcohol consumption, obesity, or renal disorders.

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

• Erythropoietin (EPO), produced by the kidney helps in erythropoiesis. 
• In kidney disease due to damage of the kidney, EPO production decreases leading to anemia.

3.What is the reason for blebs and nonhealing ulcers in the legs of this patient?

•  The reason for both is peripheral neuropathy caused by type 2 diabetes, leading to loss of sensation.
• Tight-fitting footwear, along with peripheral neuropathy in DM2, leads to bleb formation. 
• The patient may not be able to feel the friction caused by the footwear. 
• Also, diabetes causes a peripheral arterial disease that leads to decreased peripheral blood flow which delays the healing.
  
  
  
  
  
  

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

Diabetes mellitus is considered to have 4 stages

1. Insulin resistance 

2. Prediabetes

3. Type 2 diabetes mellitus 

4. Type 2 diabetes mellitus with complications

• His obesity is likely to have caused insulin resistance. 
• This later developed into frank diabetes.
• As the patient shows signs of vascular complications such as diabetic retinopathy, nephropathy and peripheral neuropathy it could be said that the patient has stage 4 diabetes mellitus. 

CASE 3C

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

QUESTIONS:

Q1. 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?

A. The event time line:

• 2-3 years ago: on and off facial puffiness 

• 1 year ago: grade 2 SOB

• 1 year ago: diagnosed with hypertension

• 2 days before admission: SOB grade 2 progressing to grade 4

• 2 days before admission: decreased urine output

    Anatomical localization of the problem: the heart: both the atria

    Primary etiology of the patients problem: congestive heart failure 

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

1. Cardivas

• MOA: nonspecific beta blocker with additional alpha 1 blocking properties

• Indication: hypertension, heart failure, post MI

• Efficacy: highly effective

2. Dytor

• MOA: torsemide: loop diuretic blocks Na+K+Cl- channels. Spironolactone: aldosterone antagonist blocks  Na+k+channel in DCT

• Indications: hypertension, heart failure, kidney failure, liver disease

• Efficacy: highly effective

3.Digoxin

• MOA: causes increased intracellular Na causes increased ca and increased contractility

• Indications: heart failure

• Efficacy: highly effective

4. Taxim:

• MOA: beta lactam antibioticacts by binding to PBP

• Indications: broad spectrum acts against many gram + and - bacteria

• Efficacy: highly effective

5.Pan D

• MOA: it is a proton pump blocker that decreases gastric acid secretion. Domperidone: D2 receptor antagonist

• Indications: acidity, GERD

• Efficacy: highly effective

6. Thiamine:

• MOA: thiamine diphosphate is a coenzyme in carbohydrate metabolism

• Indications: deficiency, wernicke's encephalopathy, beriberi

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

• The pathophysiology of cardio renal syndrome can be attributed to two broad categories of "hemodynamic factors" such as low cardiac output which was earlier considered the main reason for renal involvement due to decreased blood flow to the kidney leading to deterioration of renal function.
•  In light of new research it is now thought that elevation of both intra-abdominal and central venous pressures are the main reasons for impaired renal function.
• The patient has type 4 cardio renal syndrome.

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

The risk factors for atherosclerosis in this patient include:  

• Hypertension 

• Diabetes mellitus 

• Smoking 

• Obesity

• Physical inactivity 

• High saturated fat content in diet.

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

To make sure that the coagulatory parameters remain normal, if not to modify treatment in order to bring them to normal levels.

CASE 3D

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

QUESTIONS:

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?

• Evolution of symptomatology in patient: in 2020:the patient has had episodes of chest pain, which were relieved without medication.

• 2021 :The patient developed shortness of breath and sweating on exertion 

• Anatomical localization of the problem: coronary artery.

• Primary aetiology of patient’s problem: Atherosclerosis is the primary aetiology of the patient’s problem. An acute thrombus which leads to the obstruction of an atherosclerotic coronary artery causes Acute coronary syndrome. Which further causes myocardial infarction.

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

Pharmacological treatment: The patient was firstly given MET-XL (beta blocker)  as it decreases the oxygen demand of the heart by reducing heart rate and contractility and thus relieving the symptoms seen in the patient. It also decreases the risk of ventricular fibrillation and thus reducing incidences of sudden cardiac death.

•  When compared to the placebo given, the patients who received metoprolol had significant effect on ventricular fibrillation but the number of episodes tended to be lower in the metoprolol treated patients during the later phase.
• Non- pharmacological treatment:the patient was advised PCI.
• PCI: It is a non-surgical technique used in the treatment of obstructive coronary artery.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC59588/

https://pubmed.ncbi.nlm.nih.gov/2863148/

2) What are the indications and contraindications for PCI?

INDICATIONS:

• Acute ST-elevation myocardial infarction (STEMI)

• Non–ST-elevation acute coronary syndrome (NSTE-ACS)

• Unstable angina.

• Stable angina.

• Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)

• High risk stress test findings. 
      

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.

Source: https://emedicine.medscape.com/article/161446-overview

3) 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 overtesting and overtreatment important to current healthcare systems?

• PCI reduces the cardiovascular events in patients with acute coronary syndrome.
• If PCI is performed in a stable patient it might increase the occurrence/risk of ischemic events due to premature discontinuation of anti-platelet therapy.
•  Overtreatment continues to be a major contributor to excessive healthcare spending. When over treatment is done it might not be required and, in some cases,may even cause harmful effects on the patients rather than relieving the symptoms. Research on over treatment and over testing is necessary to put an end to unnecessary diagnostic test and provide appropriate guidelines to approach a particular symptom or disease as a whole.

Source: https://pubmed.ncbi.nlm.nih.gov/23459399/

CASE 3E

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

QUESTIONS:

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?

Evolution of symptomatology in patient: the patient has had chest pain since 3 days.

Anatomical localization: damage to the myocardial muscle(heart) due to obstruction in the coronary artery.

Etiology: Atherosclerosis is the primary etiology.

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

Pharmacological interventions:

1) Asprin: Mechanism of action: it acts by inhibiting cyclo-oxygenase and thromboxane synthase.It inhibits platelet function.

Indication: anti thrombotic effect.

Efficacy: High

2) Atrovastatin :Mechanism of action: competitive inhibition of HMG Co-A reductase. Helps in lowering LDL and IDL.

Indication: high LDL levels.

Efficacy: highest LDH-CH lowering efficacy among statins.

3) Clopidogrel: Mechanism of action: it alters surface receptors on platelets and inhibits ADP as well as fibrinogen induced platelet aggregation, it interferes with activation of platelets.

Indication: in MI

Efficacy: newer and more potent anti-platelet drug. Synergistic action when used along with asprin and prevents ischemic episodes.

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

Percutaneous transluminal coronary angioplasty, is a minimally invasive procedure that opens blocked coronary arteries to improve blood flow to the heart muscle.

CASE 3F

F) Link to patient details:

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

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

• Administration of i.v fluids in the early stages of cardiogenic shock can restore circulation by compensating for the decreased volume and perfusion. But this compensation is transient.
• Inadequate forward blood flow in a right ventricle that's compromised post-MI can lead to end-organ perfusion deficits. 
• The patient's SOB is a compensatory mechanism for the metabolic acidosis brought on by cardiogenic shock. IV bicarbonate infusion can help reverse this metabolic acidosis and temporarily alleviate SOB. 
• However, this is not the definitive treatment as IV fluids alone can cause volume overload states resulting in edema. They need to be coupled with suitable diuretics, inotropes, ACE inhibitors/ARBs

Source: https://emedicine.medscape.com/article/152191-treatment

https://www.ahajournals.org/doi/full/10.1161/JAHA.119.011991

https://www.healthline.com/health/metabolic-acidosis-treatment#treatment

2. What is the rationale for using torsemide in this patient?

Torsemide is a loop diuretic that acts on the Na+/K+/2Cl- channels in the loop of Henle. One of the adverse effects of loop diuretics is hypokalemia, which could be the reason this was chosen as the diuretic for this hyperkalemic patient.

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

• Patients with cardiogenic shock are extremely susceptible to the development of infections.
• Infections that do develop in patients with cardiogenic shock are very difficult to treat due to low perfusion states.
• As severe stasis and reduced urine output can act as a breeding ground for infectious pathogens, using prophylactic antibiotics is necessary. 

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5266423/

GASTROENTEROLOGY

CASE 4A

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

QUESTIONS:

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?

Evolution of patient’s symptomatology:

        In 2012: patient started consuming Sara.
                                               🠟                                                 

In 2017: he had pain abdomen and vomiting following which he stopped consuming sara as advised by the doctor for the next 3 years.
                                               🠟 

In 2020: he started consuming alcohol again, following which he had similar complaints of vomiting and abdominal pain.(5-6 episodes in the year)
                                               🠟 

20 days ago: increase in the consumption of alcohol.
                                               🠟    

7 days ago: last binge of alcohol following which he had vomiting diarrhoea 
                                               🠟 

4 days ago: he has had fever, constipation and burning micturition which was associated with supra pubic region.

Anatomical localization: Pancreas

Etiology: Chronic alcoholism leading to pancreatitis and a pseudocyst formation.

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?

• The main therapeutic principles for managing patients with acute pancreatitis relies on supportive care with close attention to volume status and electrolyte balance, fasting of the patient (total parenteral nutrition or naso-jejunal feeding tube), and pain management using narcotic agents(tramadol).
• Prophylactic broad-spectrum antibiotics are used to prevent infected pancreatic necrosis.
• Octreotide is a potent inhibitor of exocrine secretion of the pancreas, which plays an important role in the pathogenesis of acute pancreatitis. Octreotide also has direct anti-inflammatory and cytoprotective effects. It has therefore been suggested octreotide be used in the treatment of acute pancreatitis.
• Non pharmacological treatment: The development of peri-pancreatic fluid collections are frequent local complications in acute pancreatitis. These collections are classified as early (acute peripancreatic fluid collection or acute necrotic collection) or late (walled-off necrosis or pseudocyst). The majority of pancreatic fluid collections resolve spontaneously and do not require intervention. However, in this case as there is an infection it requires intervention.
  
  
• Interventions may include endoscopic or percutaneous catheter drainage, or in a next step endoscopic or surgical necrosectomy, minimally invasive or open.

Source:https://www.karger.com/Article/Fulltext/499631#:~:text=The%20majority%20of%20pancreatic%20fluid,necrosectomy%2C%20minimally%20invasive%20or%20open.

CASE 4B

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

QUESTIONS:

1) What is causing the patient's dyspnoea? How is it related to pancreatitis?

• Dyspnoea is caused due to inflammatory process in the lung.
• Acute pancreatitis initiates inflammatory process in the acinar cells which later progresses to generalized systemic inflammatory response syndrome. Amongst these pulmonary complications is one of the most serious one.
• Pancreatic enzymes as well as Inflammatory mediators released as a result of pancreatic injury play a key role in the pulmonary complications. The pathophysiology of ARDS is described as increased pulmonary vasculature leaking protein- rich transudate into the alveolar space and decreased lung compliance manifested clinically as refractory hypoxemia, and radiologically as diffuse infiltration in the lungs.

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

• Acute pancreatitis is associated with damage to both the endocrine and exocrine pancreas. Glucose intolerance seen with this disease appears to be the result of hyperglucagonemia and relative hypoinsulinemia. 

• Hyperglycaemia can also develop in acute pancreatitis due pancreatic oedema and the inhibitory effect of trypsin on insulin production

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

As the patient is an alcoholic, his liver enzymes might be rised. The other reason would be choledo- cholithiasis.

The biochemical markers for chronic alcohol consumption that have been most commonly studied are serum GGT, AST, ALT, mean corpuscular volume (MCV) and carbohydrate-deficient transferrin (CDT). AST to ALT ratio over 2 is highly suggestive of Alcoholic liver disease.

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

• As mentioned in the previous case, the main course of treatment for acute pancreatitis is to maintain electrolyte balance andto maintain volume status. (IVF)
• Pain management using narcotic agents(tramadol).
• ZOFER  is given which is an anti-emetic.

CASE 4C

C) Link to patient details:

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

QUESTIONS:-

1) what is the most probable diagnosis in this patient?

The most probable diagnosis is an abdominal hemorrhage secondary to a hollow viscus perforation overlapping with grade 3 renal parenchymal disease.

A ruptured hepatic abscess could also mimick a hollow viscus perforation and can cause the same sequelae. 

2) What was the cause of her death?

• The most likely cause of death in this patient is post-operative complications of emergency laparotomy.
• The patient was operated on one day before her death
• Postoperative breathlessness could be attributed to various causes such as:

1. Early (hours): Residual anesthesia, MI, hypovolemic shock, atelectasis, pulmonary embolism, fat/air embolism, fluid overload, and left ventricular failure
2. Late (hours-days): Pulmonary embolism, ARDS, infection, MI

Given the patient's history of NSAID abuse, it is likely that she died from a CVS complication or due to bleeding diathesis.

Source: https://oxfordmedicine.com/view/10.1093/med/9780198703860.001.0001/med-9780198703860-chapter-9

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

• NSAID abuse can cause nephrotoxicity in a dose-dependent fashion, decreasing the GFR, causing acute renal failure and tubular necrosis.
• NSAIDs have also been implicated in causing hypertension.

Mechanism: NSAIDs block renal protective prostaglandin (PGE2) synthesis which causes constriction of the afferent arteriole and reduces GFR. This may result in acute renal failure in low renal blood flow states.

This could have been the reason for her reduced renal compensatory mechanism which led to a low output state.
Apart from nephrotoxicity, NSAID abuse can also affect the GIT to cause ulcers and perforation; liver abscess, and thromboembolic events (which could have played a role in her post-operative complication that led to her death)

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6534025/

NEPHROLOGY

CASE 5A

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

QUESTIONS:

1. What could be the reason for his SOB?

The possible reason is due to metabolic acidosis, owing to renal failure. The compensatory response to this would be hyperventilation, presenting as SOB.

2. Why does he have intermittent episodes of drowsiness?

The most probable cause of his drowsiness and lethargy is due to hyponatremia. 

Source: https://en.wikipedia.org/wiki/Hyponatremia

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

• The patient has Acute Tubular Necrosis (ATN), which implies necrosis of the renal tubules.
• This necrosis leads to the necrosed tubules being excreted in the form of brown granular casts, which looked like a fleshy mass to the patient.
  
  
  
  4. What are the complications of TURP that he may have had?

Possible complications in this patient include: 

1. Electrolyte abnormalities

2. Pain during micturition

3. UTI

4. Urinary bladder thickening

Source: https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/transurethral-resection-of-the-prostate-turp

CASE 5B

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

QUESTIONS:

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

Hyperactivity, decreased attention span, inability to concentrate or focus on task at hand and follow instructions when seen in growing children could be attributed to various psychosomatic causes like:

• Autism
• ADHD
• Dyslexia
•  and many more (rett syndrome, tourettes etc)

The only way to reach a definitive diagnosis is to study and spend time with the child over a period of multiple sessions as psychiatric conditions take longer to arrive at a diagnosis.

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

The fact that the child has an uncontrollable urge to urinate only when he is awake could point towards a psychosomatic condition like anxiety, phobias, regression.

Such stressors are not triggered while the child is asleep hence the absence of nocturia/enuresis .

A Sleep Study in the patient should also help in determining the proportion of REM vs NREM phases , such that we can corelate whether or not he is in sound sleep or not.

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

According to the history and the investigations that were carried out ( the urine examination , culture , complete hemogram , renal profile ) were found to be within physiological limits , and also going by the spectrum of behaviour present in him ( communicated by the mother )

I'm more inclined towards a psychological quotient playing in the forefront.

Hence the mode of management is Cognitive Behavioural Therapy.

6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)  

CASE 6

A) Link to patient details:

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

QUESTIONS:

 1.Which clinical history and physical findings are characteristic of tracheoesophageal fistula?

Acquired tracheoesophageal fistula can present with repeated infections of the respiratory tract (lower>upper) such as pneumonia, hoarseness, dysphagia, cough on swallowing substances, fever of unknown origin, and chest pain.

The patient may have a history of intubation, trauma, ingestion of corrosive substances, HIV, TB, or be a known case of malignancy

The patient from the case mentioned above is:

• RVD positive
• Has had a high-grade fever for 2 months 
• Dysphagia for 2 months 
• Cough on eating/drinking for 2 months
• Hoarseness of voice
• TB positive

All these features make tracheoesophageal fistula a very likely diagnosis

Ono's sign: Intractable cough on swallowing a solid/liquid is seen in 81% of patients with an acquired tracheoesophageal fistula, including the patient mentioned above.

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

1. Given that the patient is positive for both HIV and TB and has been compliant with highly active antiretroviral therapy, there is a chance of her developing immune reconstitution inflammatory syndrome.
2. IRIS in patients with TB manifests around 2 months after the initiation of ART (the patient started ART 2 months ago, so there is a likely chance that she can develop IRIS) 
3. TB-IRIS can present initially in the form of:

• Fever                                            ✅
• Lymphadenopathy                       ❌
  
• Respiratory distress                     ✅
• Extrapulmonary complications   ✅ (disseminated TB)
  
  

TB-IRIS can be diagnosed by chest radiographs that show pulmonary nodules with worsening/new abscesses (on comparison with old radiographs) 

TB-IRIS can be prevented by promptly treating the existing TB and administering NSAIDs as IRIS is a hyperactive inflammatory immune response. In severe cases, systemic corticosteroids can be administered and if necessary, ART can be discontinued.

Sources: https://radiopaedia.org/articles/immune-reconstitution-inflammatory-syndrome

               https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3221202/

               https://academic.oup.com/bjaed/article/6/3/105/375591

7) Infectious disease and Hepatology:

CASE 7A

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

QUESTIONS: 

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

Patient history:

• This patient was diagnosed and treated for a pyogenic liver abscess. 
• He has been consuming 1 bottle of toddy/day and has smoked 10 beedis/day both for the past 30 years
• In addition to toddy he occasionally indulges in other forms of alcohol too
• Patient records don't show any history or current case of appendicitis, disorders of the hepatobiliary tree, disease of the pancreas, or gastrointestinal malignancy.
• He has no history of penetrating trauma to the abdomen
• Since this patient doesn't have a history of immunosuppressive disorders, diabetes, or recent acute infections that could have led to septicemia, the most plausible explanation for his liver abscess is chronic alcohol consumption and liver cirrhosis
  

I would like to answer the main question by answering a few others first. 

What is toddy and how much of it is too much?

• Toddy is an indigenous fermented Palm wine consumed in some south Indian states with a variable alcohol content ranging from 5-8%.
• The recommended alcohol intake per day is 10–42 g/day or 98–140 g/week for women and 10–56 g/day or 150–280 g/week for men [1] https://pubmed.ncbi.nlm.nih.gov/27073140/
  
• This means the patient could have potentially exceeded the daily limit for alcohol consumption (assuming a bottle is 750ml in this case) 

Is toddy the culprit? 

• While chronic alcohol consumption alone can be a risk factor for the formation of a liver abscess, chronic indigenous alcohol consumption has been specifically linked to an increase in amoebic liver abscess. Amoebae were not isolated from the aspirate of this patient

What could have caused it?

• Pyogenic liver abscesses are common in cases of liver cirrhosis but the fact that the patient's SGPT and SGOT were in the normal range during follow up indicates that he might not have had liver cirrhosis and the initial elevation in liver enzymes was due to the abscess itself 
• Consistently elevated ALP before treatment and throughout follow up could point to an involvement of the hepatobiliary tree
• Pyogenic liver abscesses where only a single organism can be isolated from the aspirate( such as the one seen in the patient) are more likely due to hematogenous spread of bacteria from a pre-existing focus of infection

Conclusion: I believe the cause of this patient's abscess might have been due to various factors such as pre-existing infections, suppressed immunity, toxic injury to the liver that were all driven by chronic alcoholism, and that toddy, in particular, did not increase the risk for pyogenic abscess as compared to other forms of alcohol

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

• Chronic alcoholism can significantly suppress one's immunity
• Alcohol+smoking both cause injury to normal hepatocytes
• Chronic alcohol use over a period of 10-20 years can consistently blunt normal liver physiology and histology by bringing about cirrhotic changes in the liver and cirrhosis, in turn, increases the risk of developing liver abscesses (even though only 10-15% of alcoholics develop cirrhosis).

3. Is liver abscess more common in the right lobe?

Yes, an abscess of the right lobe is twice as common as the left due to the anatomical distribution of the blood supply of the liver.
Right hepatic lobe: 1) Right hepatic artery
                               2) Superior mesenteric vein

                               3) Portal veins
Left hepatic lobe: 1) Left hepatic artery
                              2) Inferior mesenteric vein

                              3) Splenic drainage

It also accounts for more hepatic mass compared to the left lobe (6:1) and hence has a larger network for both blood supply and biliary canaliculi

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

1.  Abscess of the left lobes: More susceptible to rupture than abscesses of the right lobe
2. To confirm a diagnosis
3.  Abscesses in uncommon locations
4.  Large abscesses (>6cm)
5.  High fever that doesn't respond to antipyretics
6.  Toxaemia 
7.  Abscesses that don't respond to drug therapy/conservative treatment
8.  Expanding abscess
9.  Complications: Rupture into the peritoneum, pericardial space, pleural cavity, or through the anterior abdominal wall

CASE 7B

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

QUESTIONS:

1) Cause of liver abscess in this patient?

• The patient has an elevated titer of Alkaline phosphatase while his AST and ALT are within range. 
• His thin build, complaints of fever and pain for 20 days, and LFT findings all point towards a chronic course of the disease. This could be due to an unresolved liver abscess persisting and carrying out a slightly indolent course.
• The cause of the abscess the very first time could be pyogenic or amoebic. Given that a single hyperechoic mass was visualized on the abdominal USG, it was most likely an amoebic liver abscess.
• The patient's abscess responded well to treatment with metronidazole which is the drug of choice for amoebic liver abscess
• Amoebic liver abscesses have been linked to toddy consumption

2) How do you approach this patient?

Medical management: 

1. Antibiotics: Metronidazole, paromomycin, diloxanide furoate+broad spectrum antibiotics (for secondary infections/ if it's a pyogenic abscess) 
2. Analgesics: NSAIDs, opioid analgesics (in cases of severe pain)
3. Antipyretics: Paracetamol
4. USG guided aspiration: Done in select cases such as abscess>6cm, refractory to conservative treatment, high-grade fever not responding to antipyretics or an abscess of the left lobe

Surgical management: 

Surgical drainage by transperitoneal or posterior transpleural can be done in cases of thick-walled multiloculated abscesses, failure of previous attempts to drain via aspiration, peritonitis

3) Why do we treat here; both amoebic and pyogenic liver abscess? 

As serological tests were not carried out for this patient, there is no definite way to diagnose the nature of the abscess. Hence, the patient should be treated for both pyogenic and amoebic abscess as a part of conservative medical management. 

Pyogenic liver abscesses are usually caused by streptococcus sps, , E. coli or Klebsiella pneumonia, and metronidazole alone does not effectively cover these organisms. On the other hand, broad-spectrum antibiotics like cephalosporins or quinolones alone are ineffective against amoebic abscesses. Hence, a combination of the two will be the most effective in treating the infection.

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

Yes.

CT scan is the preferred modality for the detection of a liver abscess.

However, to differentiate a pyogenic liver abscess from an amoebic one, the following tests can be carried out: 

1. Blood culture: Useful for diagnosis of a pyogenic liver abscess. Less invasive and risky compared to fine-needle aspiration of the abscess
2. Serological tests: For Entamoeba antigens, more useful in non-endemic regions
3. Aspiration: The appearance of the aspirate from the abscess can give us an idea about the pathogen causing the abscess. Amoebic liver abscess aspirates have an anchovy paste appearance (brown, thick odorless) while aspirate from a pyogenic abscess is usually purulent and malodourous. This is not the most reliable test.
4. Culture of aspirate: Gold standard for diagnosis of a pyogenic liver abscess
5. Molecular testing of the abscess aspirate: reliable in the diagnosis of amoebic liver abscess, but costly

INFECTIOUS DISEASE (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)

CASE 8

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

QUESTIONS:

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 aetiology of the patient's problem?

Evolution of symptomatology:

In 2019: patient was diagnosed with hypertension

                                         🠟

18/04/21 : he took COVAXIN following which he had fever the same night.

                                         🠟

28/04/21: he had generalized weakness and facial puffiness and perioritaledema.04/05/21: he had altered sensorium and had weakness in right upper and lower limb.

Anatomical localization: Orbit, nose, oral cavity, pancreas, left frontal and temporal lobe

Etiology: Diabetic ketoacidosis promoting infection with mucormycosis.

• In the presence of hyperglycemia and low pH, which is found in patients with diabetic ketoacidosis (DKA), phagocytes are dysfunctional and have impaired chemotaxis and defective intracellular killing by both oxidative and nonoxidative mechanisms.
• This promotes infection with mucormycosis in the presence of compromised immune system of the host.

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?

• Lipid formulations of amphotericin B (LFAB) are the drug of choice to treat mucormycosis. 

• Adjunctive therapy: Recombinant cytokines, hyperbaric oxygen, and/or granulocyte transfusions can be considered for selected patients. Early initiation of therapy is critical to maximizing outcomes.

• Surgical approach:  surgical debridement; “aggressive-conservative” approach- frozen sections are used to delineate the margins of infected tissues, and uninvolved tissues are spared from debridement when possible.

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

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

Mucormycosis is an opportunistic fungal infection. That means it infects people who have a weak immune system, that includes diabetic patients, patients taking corticosteroids, and other conditions. As there is a recent surge in the COVID-19 cases, steroids are being used to treat it. This increases the chances of the patients acquiring mucormycosis post COVID due to the immune-compromised state caused by the usage of steroids. 

At the same time, it has been noted that diabetic patients who have contracted COVID have a severe course of disease leading to the usage of steroids for a long time. All such reasons have led to a sudden increase in the incidence of mucormycosis in India.

9) INFECTIOUS DISEASE (Covid 19)

http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1

CASE 9-1

1) Covid 19 with comorbidity (Pulmonology/Rheumatology)

https://nikhilasampathkumar.blogspot.com/2021/05/covid-pneumonia-in-pre-existing-case-of.html

Questions: 

1) How does the pre-existing ILD determine the prognosis of this patient?

1. The pre-existing ILD significantly worsens the prognosis of this covid patient. 
2. Interstitial lung disease is characterized by dyspnea, decreased pulmonary diffusing capacity, decreased FVC and TLC. The SpO2 of these patients is usually decreased due to increased A-a gradient
3. A superimposed covid-19 infection in these cases can cause an acute exacerbation of symptoms such as dyspnea, decreasing levels of SpO2 further and faster than in Covid-19 patients without interstitial lung disease. 
4. Radiology (HRCT) usually shows the development of new pulmonary opacities and fibrosis.

Patient factors: 

• Since this patient already had a reduced SpO2 of 90-92% (compared to the normal range of >96%) she is more susceptible to worsening of hypoxia and dyspnea unless immediate ventilator support is provided
• The patient reportedly did not have dyspnea prior to the covid infection but developed a grade 2 SOB
• ILD by itself makes the patient much more susceptible to acquiring Covid-19 infection.

Prognosis: Poor

Source: https://ejrnm.springeropen.com/articles/10.1186/s43055-021-00431-2

2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism? 

• Low-dose steroids for short intervals of time have been shown to be the most effective way of using steroids to treat RA. A dose of <10mg/day is considered safe and ideal when coupled with DMARDs. High-dose steroids like the ones used to treat severe covid cases will be counterproductive in a rheumatological POV and can flare up the disease.
• High-dose pulse therapy with methylprednisolone or other glucocorticoids can be almost fatal in cases of Hashimoto's disease, as seen in some cases of Hashimoto thyroiditis that developed autoimmune hepatitis.

Sources: https://rmdopen.bmj.com/content/6/1/e000536

https://thyroidresearchjournal.biomedcentral.com/articles/10.1186/s13044-019-0074-0

3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?

• An individual history of autoimmune diseases and family history (HLA) makes an individual more susceptible to developing other autoimmune conditions. 
• The development of autoimmune conditions subsequent to COVID-19 infection could be related to: 

1. Transient immunosuppression of innate and acquired immunity 
2. Loss of self-tolerance to self-antigens
3. A form of inappropriate immune reconstitution in individuals with predisposing conditions of autoimmunity.

Mechanism: 

• The immunosuppression that occurs during a SARS-CoV-2 infection, as well as the redistribution of immune system cells, could be associated with a transitory decrease in the sentinel effect monocytes, macrophages, and dendritic cells by which they identify self-cells against which they would not react and non-self cells against which an immune/inflammatory response would be triggered.
• This could possibly lead to loss of self-tolerance towards some self- antigens.
• This transient immunodeficiency occurs during the disease, as well as a form of immune reconstitution in convalescence.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7556280/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150011/

4) Why was she prescribed clexane (enoxaparin)?

• The main pathogenesis of systemic inflammation caused by Covid-19 is by inducing a cytokine storm that causes epithelial cell necrosis, increased vascular permeability, dysfunctional humoral and CMI which all collectively lead to acute lung injury and ARDS
• Of these cytokines, IL-6 is one that is the most important in determining the prognosis. IL-6 levels are highly elevated in patients with severe disease
• Enoxaparin is said to relieve and prevent inflammation produced by IL-6 by inactivating it by binding it with its non-anticoagulant fraction, especially in pulmonary epithelial cells.
• Moreover, patients with Covid-19 are more susceptible to the development of venous thromboembolism, which can be prevented by Enoxaparin (LMWH)
  
  
  
  
  

Source:https://www.frontiersin.org/articles/10.3389/fphar.2020.579886/full

CASE 9-2: COVID-19 SEVERE

https://nehapradeep99.blogspot.com/2021/05/a-50-year-old-female-with-viral.html

QUESTIONS:

1) Since the patient didn't show any previous characteristic diabetes signs, did the Covid-19 infection aggravate any underlying condition and cause indolent diabetes to express itself? If so what could be the biochemical pathways that make it plausible?

The patient may have already had slight hyperglycemia, owing to high HbA1c levels (7.1%), which may have aggravated due to COVID-19. The possible biochemical pathways include:

• Altering glucose metabolism
• RAAS pathway
• Modulating immune response
• Increasing susceptibility to thromboembolic/bleeding events

 

Source: https://www.nature.com/articles/s41574-020-00435-4#:~:text=Initial%20studies%20found%20increased%20severity,predispose%20infected%20individuals%20to%20hyperglycaemia

2) Did the patient's diabetic condition influence the progression of her pneumonia?

Yes, DM or hyperglycemia in patients leads to an increase in COVID-19 severity. Also, poor glycaemic control predicts an increased need for medications and hospitalizations, and increased mortality.

In monocytes: elevated glucose levels increase SARS-CoV-2 replication, and glycolysis sustains SARS-CoV-2 replication via the production of mitochondrial reactive oxygen species and activation of hypoxia-inducible factor 1α. Therefore, hyperglycemia supports viral proliferation.

3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?

D- Dimer levels indicate the severity of COVID-19, pertaining to possible thrombotic complications- as D Dimer is formed post- fibrinolysis.

D- Dimer does change the management, as D-Dimer levels above 2000ng/dl were found to have a direct link with the increasing severity of COVID-19. Moreover, D- dimer levels would be helpful in fast diagnosis and prevention of thrombotic complications.

Source: https://journals.lww.com/md-journal/fulltext/2020/11130/trends_and_diagnostic_value_of_d_dimer_levels_in.65.aspx

CASE 9-3 (COVID-19 SEVERE)

https://143vibhahegde.blogspot.com/2021/05/covid-in-26-yo-female.html

QUESTIONS:

1. Why was this patient given noradrenaline?

Following kidney failure, the patient had sudden and persistent hypotension. To combat this, the patient was given noradrenaline, a potent vasoconstrictor.

2. What is the reason behind testing for LDH levels in this patient?

LDH (Lactate Dehydrogenase) catalyzes the conversion of lactate to pyruvate and back. Hence, an increase in LDH denotes some form of tissue damage. In this patient, an increase in LDH levels would denote inflammation, and a high increase would denote Multi-Organ Failure.

3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?

Although BiPAP is a positive pressure system, unlike tracheal intubation, it does not send the air to the trachea and depends on the patient's ability to respire. In this patient, as SpO2 levels were dropping to 30% despite BiPAP, a more invasive method was required to push the air directly into the lungs- hence intubation was preferred.

CASE 9-4 (COVID-19 MILD)

https://gsuhithagnaneswar.blogspot.com/2021/05/29-year-old-male-patient-with-viral.html?m=1

QUESTIONS:

1. Is the elevated ESR due to COVID-related inflammation? 

Yes, as ESR is an important indicator of immunological loss and owing to increased inflammation and immunological dysfunction in COVID, elevated ESR is most likely due to COVID-related inflammation. 

2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and the harms of hospitalization?

Hospitalization was due to Grade 3 Shortness of Breath (SOB), and the long duration of COVID-19 infection.

Challenges of home isolation-

1. Physical challenges- Many patients may find it hard to cut themselves from the outside world and confine themselves to a room for long periods of time

2. Emotional challenges- Sitting in a small room all day leads to stress, anxiety, and even depression, with an increase in mental health issues being reported during the pandemic

3. Social challenges- Members of society who cannot care for themselves on their own (eg, patients with disability, geriatric patients, etc) are at a major loss 

4. Economic challenges- Some patients, such as daily wage laborers, cannot afford to home isolate themselves as they need to earn on a daily basis to keep their family going

Harms of hospitalization:

1. Infection- Members visiting may get COVID from exposure to the hospital ward alone

2. Cost- PAtient may not be able to bear the brunt of high costs

3. Overtesting- Hospitals may ask the patients to stay overnight despite the conditions being mild, based on preliminary test results

4. Economic- Working patients may have to take a leave of absence, hence affecting both their work and decreasing their salary, on top of spending money on hospitalization

         

CASE 9-5 (COVID-19 SEVERE)

https://anuragreddy72.blogspot.com/2021/05/case-discussion-on-hypokalemic-periodic.html

QUESTIONS:

1) What was the reason for the coma in this patient? 

The reason for the coma is due to severe hypoxia, as his SpO2 levels were 20% when he was admitted. Along with this, hypokalemia leads to respiratory muscle paralysis, which may have aggravated his dyspnoea.

2) What were the competency gaps in hospital 1 Team to manage this intubated comatose patient that he had to be sent to hospital 2? Why and how did hospital 2 make a diagnosis of hypokalemic periodic paralysis? Was the coma related? 

The main competency gap was in the lack of testing for serum electrolytes, as the hypokalemia had caused weakness and fatigue in this patient. 

• Hospital 2 makes a diagnosis of hypokalemic periodic paralysis based on the fact that the patient had generalized weakness before becoming comatose, along with tingling and symptoms of paralysis. On testing serum electrolytes, his potassium levels were found to be 2.3 mEq/L (normal-3.5-5)
• The coma was most probably related, as hypokalemia can cause respiratory muscle paralysis, leading to aggravation of hypoxia, hence causing unconsciousness in the patient. 

3) How may COVID 19 cause coma?

• Yes, as the brain is extremely sensitive to oxygen, oxygen deprivation due to COVID-19 can lead to a comatose state.
• This patient had very low SpO2 levels (20%), which may have caused the coma.

CASE 9-6 (COVID-19 WITH ALTERED SENSORIUM)

https://vijaykumarkasturi.blogspot.com/2021/05/65-years-old-male-with-viral-pneumonia.html

QUESTIONS:

1. What was the cause of his altered sensorium?

Probable causes: 

1. Altered sensorium due to hypoxia, leading to hypercapnic encephalopathy and altered sensorium

2. Increased urea levels leading to uraemic encephalopathy, which causes altered sensorium

2. What was the cause of death in this patient?

The cause of death in this patient was due to complications of COVID-19, most probably Acute Kidney Failure (AKI), as denoted by increased urea and creatinine, and hypoproteinemia. Hypoxia and inflammatory response due to COVID-19 may have triggered the process.

CASE 9-7

https://drsaranyaroshni.blogspot.com/2021/05/a-67-year-old-lady-in-icu-with-covid.html

QUESTIONS:

1) What is the grade of pneumonia in her?

Based on the CT severity score it can be said that the patients pneumonia is moderate.

2) What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?

It is best to start the treatment with dexamethasone before the onset of cytokine storm.

3) What all could be the factors that led to psychosis in her ?

The following can lead to ICU psychosis

• Sensory deprivation

• Sleep deprivation

• Stress

• Continuous light levels 

• Continuous monitoring

• Lack of orientation

• pain

• drug reactions

• Infections

• metabolic disorders

• Dehydration

4) In what ways shall the two drugs prescribed to her for psychosis help?

Pirecetam improves memory and causes cognitive enhancement and also improves mood.

Resperidone acts by decreasing the dopaminergic and seritonergic pathways in the brain

5) What all are the other means to manage such a case of psychosis?

• The management of ICU psychosis primarily depends on the cause. If it is sleep deprivation then hte patient should be provided a peaceful place to take rest.
• If it is due to underlying conditions like heart failure and dehydration then these should first be corrected. 
• Haloperidol is a medication commonly used to manage ICU psychosis. Other common anti-psychotics can also be used.

6) What all should the patient and their attendants be careful about ( w.r.t. COVID )after the patient is discharged ?

The patient is supposed to self isolate after they are discharged for another 7 days after discharge. If possible oxygen levels are to be monitored as well for the next 7 days. The patients and the patient's attenders should be on the look out for danger symptoms such as 

trouble breathing, chest pain, bluish discolouration of lips, confusion or inability to wake up.

7) What are the chances that this patient may go into long covid given that her "D Dimer" didn't come down during discharge? 

Long COVID is the persistence of symptoms such as cough, breathlessnes, headaches and chest pain weeks to months after discharge. People suffering from long COVID usually have elevated biomarkers such as elevated d dimer and CRP. As this patient has elevated d dimer levels at discharge there is a good chance that she could suffer from long COVID.

CASE 9-8

https://bhavaniv.blogspot.com/2021/05/35yrm-with-viral-pneumonia-secondary-to.html?m=1

QUESTIONS:

1) Can psoriasis be a risk factor for severe form of COVID?

There is no evidence that patients with moderate-to-severe psoriasis receiving systemic treatments, including biologics, have higher risk of SARS-CoV-2 infection and/or increased hospitalization and death related to COVID-19 compared to the general population.

2) Can the increased use of immunomodulatory therapies cause further complications in the survivors?

Immunomodulators help COVID 19 patients by suppressing the cytokine storm  but they also have thepotentialt to increase the risk of infection  (like mucormycosis), traditional clinical signs may be masked with resulting delays in identification and treatment. 

3) Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?

Increasing evidence from experimental and clinical studies suggests that mechanical ventilation, which is necessary for life support in patients with acute respiratory distress syndrome as seen in COVID 19  can cause lung fibrosis, which may significantly contribute to morbidity and mortality. It is believed that ventilator induced lung injury is the cause for the fibroproliferative changes and the resultant lung fibrosis.

CASE 9-9

https://vidya36.blogspot.com/2021/05/a-45-year-old-female-with-viral.html

QUESTIONS:

1) What is the type of DM the patient has developed ?(is it the incidental finding of type 2 DM or virus induced type 1DM)? 

• Incedental type 2 DM can be differentiated from de novo covid induced type 1 DM with the help of the HbAc1 levels.
• As HbAc1 levels are indicators of long term blood ssugar levels they are likely to be raised in pre existing DM that was incidentally discovered. But in case of the diabetes being de novo in nature then the HbAc1 levels are unlikely to be raised. 
• As the patients HbAc1 levels are not raised we can not at this point determine if the patient has incedental discovered type 2 DM or Covid induced de novo DM.

2) Could it be steroid induced Diabetes in this patient?

As the patient was given dexamethasone as a part of her treatment regimen it is possible that her elevated glucose levels are a result of steroid induced hyperglycemia.

CASE 9-10

https://vidya36.blogspot.com/2021/05/comparative-study.html?m=1

QUESTIONS:

1) What are the known factors driving early recovery in covid?

The following factors can lay a role:

• Younger age group

• shorter duration of fever 

• No diabetes

• PaO2/FiO2 levels

• No comorbidities

CASE 9-11

https://rishithareddy30.blogspot.com/2021/05/covid-case-report.html

QUESTIONS:

1) How is the diabetes related to the prognosis of COVID patients? What are the factors precipitating diabetes in a patient developing both covid as well as Diabetes for the first time? 

People suffering from diabetes are like to experience more severe symptoms of the disease than the ones who are not diabetic. Even within the patients that are diabetic the people whose disease is under better control tend to have a better prognosis.

Possible causes for de nov diabetes in COVID19 include:

 

• The SARS CoV 2 virus enters the cells through the ACE 2 receptors which are present in large  numbers in the pancreas
• and that this damages the pancreatic cells.
• Another theory is that the inflammation caused by the cytokine storm damages the beta cells.

2) Why couldn't the treating team start her on oral hypoglycemics earlier?

As the insulin is faster acting as compared to oral hypoglycemics and as her blood glucose level was very high it is important to bring it down as fast as possible.

CASE 9-12

12) Moderate to severe covid with prolonged hospital stay:

https://93deepanandikonda.blogspot.com/2021/05/42-years-female-patient-with-viral.html

QUESTIONS:-

1) What are the potential bio clinical markers in this patient that may have predicted the prolonged course of her illness? 

Serum LDH: 571U/L      (Normal range=140-280U/L
ALP : 342 U/L                (Normal range=44-147U/L)

SpO2: 82% at RA           (Normal range= >96%)

HR: 124bpm                   (Normal range=60-100bpm)

Classically, the bio clinical markers that are predictive of a Covid-19 patient's outcome are

• C reactive protein [>57.9mg/dL]
• D-Dimer [>1mcg/ml associated with poorer prognosis]
• Serum LDH [>248U/L]
• IL-6 [2.9 times higher in severe disease compared to mild disease]
• SGPT [Isolated rise in SGPT >3 times the normal value]
• ESR [high sustained level after recovery from infection]
• Albumin
• Platelet count 
• Neutrophil count
• NLR: [>5.5]
• Urea
• Creatinine
• High sensitivity Troponin

The patient in question has elevated levels of serum LDH and ALP. Her CRP and D-Dimer levels are not high enough to be considered as a bad prognostic factor.

Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219356/

               https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7194951/
               https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7896696/

CASE 9-13

13) Severe covid with first diabetes 

https://vignatha45.blogspot.com/2021/05/58-years-female-patient-with-viral.html

1) What are the consequences of uncontrolled hyperglycemia in covid patients?

• Hyperglycemia can lead to anomalous glycosylation of tissue receptors throughout the body. One of these receptors happens to be ACE2, the same receptor SARS-CoV2 uses to gain entry into the host cell. In fact, glycosylation of ACE2 is necessary for the virus to establish an infection.
• Uncontrolled hyperglycemia freely facilitates this glycosylation, making these patients more susceptible to Covid-19 infections and increasing the severity of the infection by helping increase the viral load (by increasing the concentration of glycosylated ACE2) 
• Control of blood sugar can also decrease the chances of a cytokine storm during the second phase of the infection.
• Uncontrolled hyperglycemia hence, suggests a poor prognosis in Covid-19 patients.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7188620/#:~:text=Therefore%2C%20high%20and%20aberrantly%20glycosylated,and%20a%20higher%20disease%20severity.

2) Does the significant rise in LDH suggests multiple organ failure?

Lactate dehydrogenase has 5 isoenzymes that are present in various tissues such as the heart, RBCs, lungs, liver, kidney, brain, and skeletal muscle.

Since covid-19 primarily causes lung damage, LDH3 is released into the blood giving an elevated titer.

Multi-organ damage that involves the heart (myocarditis) or kidneys (renal failure) can lead to an elevation in respected isoenzymes found in these tissues.

Hence, a significant rise in LDH indicates a poor prognosis and points towards multi-organ damage.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7251362/

3) What is the cause of death in this case?

This patient was diagnosed with uncontrolled hyperglycemia with severe covid pneumonia.

LFT shows elevated AST, ALT, and ALP with a gross increase in bilirubin titer. 

The D-Dimer is elevated (560ng/ml) and the LDH is 835U/L both of which are indicators of a poor prognosis. 

The most likely cause of death in this patient seems to be ARDS. 

The immediate cause of death: Most probably cardio-pulmonary arrest

Antecedent cause: Severe covid-19 pneumonia

CASE 9-14

14) Long covid with sleep deprivation and  ICU psychosis 

https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html

QUESTIONS:

1)Which subtype of ICU psychosis did the patient land into according to his symptoms?

Hyperactive delirium: Manifests as agitation, restlessness, refusal to cooperate with caregivers, unprovoked mood changes, hallucinations

2)What are the risk factors in the patient that has driven this case more towards ICU psychosis?

• Hypertension
• History of cerebrovascular accident (makes him more prone to a new one)
• Steroid use
• Sedative use (Gabapentin)
• COPD

3)The patient is sleep-deprived during his hospital stay. Which do you think might be the most probable condition?

 A) Sleep deprivation causing ICU psychosis

 B) ICU psychosis causing sleep deprivation 

B) ICU psychosis causing sleep deprivation is more likely in this patient

4) What are the drivers toward current persistent hypoxia and long covid in this patient? 

Elevated bio clinical markers like D-Dimer, LDH, Neutrophils, WBCs(absolute), IL-6, and CRP all contribute to persistent hypoxia and worsen the prognosis. In addition to this, ICU psychosis adds to the prolonged hospital stay.

CASE 9-15

15) Moderate Covid with comorbidity (Truncal obesity and recent hyperglycemia) 

https://meghanaraomuddada.blogspot.com/2021/05/case-1-2021-42yr-old-male-with-fever.html

QUESTIONS: 

1. As the patient is a non-diabetic, can the use of steroids cause a transient rise in blood glucose?

Cortisol stimulates gluconeogenesis in the liver and inhibits glycogen synthesis, increasing blood glucose. Continuous treatment with corticosteroids can lead to elevated blood glucose titers even in non-diabetics.

2. If yes, can this transient rise lead to long-term complications of New-onset diabetes mellitus? 

It is still unclear if the alterations brought about by covid-19 in the glucose metabolism are permanent and persist or remit after the resolution of infection. There are ongoing studies that aim to answer these questions.

Steroid diabetes is a term coined to describe diabetes mellitus arising as a result of glucocorticoid use for more than 50 years

3. How can this adversely affect the prognosis of the patient?

 Hyperglycemia in general is indicative of a poorer prognosis in a patient compared to covid patients with normal blood glucose levels.

4. How can this transient hyperglycemia be treated to avoid complications and a bad prognosis?

Oral hypoglycemics (such as sulfonylureas) are efficient at controlling blood glucose levels in non-diabetics who develop steroid-induced hyperglycemia. Most cases revert to normoglycemia after discontinuation of steroids.

5. What is thrombophlebitis fever? 

Fever in response to thrombophlebitis that is caused due to release of inflammatory mediators 

6. Should the infusion be stopped in order to control the infusion thrombophlebitis? What are the alternatives?

No, infusion thrombophlebitis is not grounds for discontinuation of infusions that are essential for the treatment of the case. Thrombophlebitis can be treated by local compressive dressings, NSAIDs (topical and/or systemic)

CASE 9-16

16) Mild to moderate covid with hyperglycemia 

https://vaishnavimaguluri138.blogspot.com/2021/05/viral-pneumonia-secondary-to-covid-19.html

QUESTIONS:

1. What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?

The possible factors that could have led to precipitation of diabetes in a covid-19 patient are:

• Genetic susceptibility to diabetes
• Pre diabetic state
• Viral insult to the beta cells of the pancreas
• Stress hyperglycemia due to inflammation-induced insulin resistance
• High dose steroid usage

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7669477/

2. What is the frequency of this phenomenon of New-Onset Diabetes in Covid Patients and is it classical type 1 or type 2 or a new type?

Italy, early 2020:  23% fewer annual cases of new childhood diabetes were reported. Of these, the cases with DKA were more severe compared to cases with DKA from 2019(44.3% vs. 36%, respectively) [68 Germany: There was a  two-fold increase in DKA in children and adolescents during the COVID-19 pandemic 

UK reported an increase in the referral of children with DKA when compared with previous years. A more recent multicenter study from the UK describes an apparent increase in new-onset T1DM in children, with evidence of SARS-CoV-2 infection or exposure in some of these.

Most of these cases were DM-1 or mimicked DM-1 in children. However, on the whole, it is unclear if most of these cases were of DM-1, DM-2, or of a new type.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7669477/

3. How is the prognosis in such patients? 

New-Onset Diabetes is associated with a worse prognosis in Covid-19 patients compared to normoglycemic patients due to a possibility of increased viral load and development of cytokine storm.

These patients are prone to developing DKA and hyperosmolar syndromes

Their prognosis is comparable to those of patients with pre-existent diabetes.

Source: http://covidiab.e-dendrite.com/introduction.html

4. Do the alterations in glucose metabolism that occur with a sudden onset in severe Covid-19 persist or remit when the infection resolves?

It is still unclear if the alterations brought about by covid-19 in the glucose metabolism are permanent and persist or remit after the resolution of infection. There are ongoing studies that aim to answer these questions

Source: http://covidiab.e-dendrite.com/introduction.html

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7304415/

5) Why didn't we start him on Oral hypoglycemic agents earlier? 

The patient's HbA1c was checked late (on the 2nd/3rd day of admission) which was the reason for the delay in administering glimepiride.

Source: Data obtained on contacting the person who logged the case

CASE 9-17

https://prathyushamulukala666.blogspot.com/2021/05/a-62-year-old-male-patient-with-fever.html

QUESTIONS:

1)Does hypertension have any effect to do with the severity of the covid infection. If it is, Then how?

Yes, hypertensive patients are at a higher risk of COVID 19 severity. It is already known that hypertension is associated with a weaker immune system and is seen in older patients which show a bad prognosis when dealing with this infection. As there is a high risk of developing cardiovascular events as well as end-organ failure.

2)What is the cause for pleural effusion to occur?

Pneumonia caused due to COVID-19 infection lead to increase the permeability of microvascular circulation which lead to pleural effusion(exudative type)

CASE 9-18

https://meesumabbas82.blogspot.com/2021/05/a-38-yo-male-with-viral-pneumonia.html

QUESTIONS:

1. What is the reason for hypoalbuminemia in the patient?

The reason for hypoalbuminemia in COVID_9 patient is due to increased catabolism of albumin to make amino acids as well as a simultaneous decrease in albumin synthesis( albumin is a negative acute-phase reactant that means its level decrease during inflammation)

2. What could be the reason for exanthem on arms? Could it be due to covid-19 infection?

     Exanthem is an eruptive skin rash seen in viral infections. Yes, this could be due to COVID-19 infection. The exanthem in COVID-19 resembles that of varicella.

3. What is the reason for Cardiomegaly?

High blood pressure might be the underlying cause for cardiomegaly in this patient.

Uncontrolled high blood pressure leads to an increase in the workload of the heart. To compensate for this demand, the ventricles undergo remodeling leading to cardiomegaly.

4. What other differential diagnoses could be drawn if the patient tested negative for covid infection?

• Chickenpox

• Shingles

• Pytriasis

5. Why is there an elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?

• D-dimer is increased in a COVID-19 patient. It may be related to the viral life cycle. 
• The apoptotic processes target the endothelial cells of the vasculature resulting in triggered coagulopathy and ultimately result in increased d-dimer levels.

CASE 9-20

https://srilekha77.blogspot.com/2021/05/a-48-year-male-with-viral-pneumonia-due.html

QUESTIONS:

1)Can usage of steroids in diabetic Covid patients increases the death rate because of the adverse effects of steroids?

• COVID-19 infection causes systemic inflammation and cytokine storm. In order to prevent these severe conditions steroids are used.
• A well-known adverse effect of steroid usage is the disruption in carbohydrate metabolism. It leads to hyperglycemia. When steroids are given to a diabetic COVID-19 patient utmost care must be taken. 
• The patient should be shifted from oral anti-diabetic drugs to s.c. insulin and blood sugars should be closely monitored.
• If possible, Tocilizumab should be used instead of steroids.
• Steroid usage in a diabetic patient has shown an increase in death rate as it further decreases the immunity of the patient and makes them prone to other opportunistic infections like mucormycosis that leads to an increased death rate.

2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically?

• In COVID-19 infection due to systemic inflammation and cytokine storm even when they are adequately managed, ae leading to damage of inner walls of small blood vessels of the brain. These blood vessels have very little or no collateral blood supply. 
• Even though the patient is on blood thinners they cannot prevent this damage. When the blood viscosity becomes higher either due to dehydration or high LDL/cholesterol levels, these small blood vessels are blocked leading to stroke.

3)Does chronic alcoholism have an effect on the outcome of Covid infection? If yes, how?

Yes, chronic alcoholism does worsen the prognosis of the COVID-19 patient.

One of the adverse effects of chronic alcoholism is its ill effect on innate as well as adaptive immunity.

Reduced resistance to COVID-19 promotes progression of the disease and leading to a worse prognosis

CASE 9-21

https://sudhamshireddy.blogspot.com/2021/05/a-65-year-old-female-with-fever.html

QUESTIONS:

1. What can be the causes of early progression and aggressive disease(Covid) among diabetics when compared to non-diabetics?

It is observed that there is an early as well as aggressive progression of COVID 19 in diabetics. This is attributed to interactions of several risk factors as well as hyperglycemia which is seen in diabetic patients. It modulates immune response as well as inflammatory responses thus predisposing individuals to lethal course of the disease.

2. In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?

Methylprednisolone from 40 mg/day to 160 mg/day for 6 days according to the weight and status of the patients. During this course of treatment, blood sugar should be closely monitored and the patient should be shifted from oral anti-diabetic drugs to insulin.

3. What effect does a history of CVA have on COVID prognosis?

It is established that COVID-19 is associated with coagulopathy. Patients who have a history of CVA are mostly old and have other co-morbidities which leads to a severe course of the disease as well as poor prognosis.

CASE 9-23

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-viral-pneumonia.html

QUESTIONS:

1) What do you think are the factors in this patient that are contributing to his increased severity of symptoms and infection? 

• Old age

• Diabetes mellitus type 2

• Chronic kidney disease

• Bronchial asthma

2) Can you explain why the D dimer levels are increasing in this patient? 

It may be related to the viral life cycle. The apoptotic processes target the endothelial cells of the vasculature resulting in triggered coagulopathy and ultimately result in increased d-dimer levels

3) What were the treatment options taken up with falling oxygen saturation? 

• Head elevation

• Self proning

• O2 supplementation

4) Can you think of an appropriate explanation as to why the patient has developed CKD, 2 years ago? (Note: Despite being on anti-diabetic medication, there was no regular monitoring of blood sugar levels and hence no way to know for sure if it was being controlled or not)

During the early stage of diabetes, there is an increase in blood flow to the kidneys, which strains the glomeruli and lessens their ability to filter blood. High levels of glucose in the blood lead to the accumulation of extra material (abnormal glycation of RAGE receptors) in glomeruli. It increases the stress of glomeruli in turn leading to gradual and progressive scarring. Eventually leads to the development of CKD.

MASTER CHART FOR COVID PATIENTS FOR THE MONTH OF MAY, 2021

Link to the master chart prepared by me:  

https://docs.google.com/spreadsheets/d/1RoTcL9cS6aJRez88WDQYBQbMgY170XP0gwqX6brI3Kc/edit?usp=sharing

10) MEDICAL EDUCATION

MEDICAL EDUCATION

MAY 2021 LOG:

11TH: Studied about types of seizures and pharmacological treatments.

12TH: Studied ECG and tried to identify the common abnormalities seen in the waveform

14TH: Read about a case of a 65year old with acute coronary syndrome that was posted by a batchmate and reviewed literature surrounding PCI. 

16TH: Read about neurological examination and types of delirium in ICU patients

17TH: Took up a case of GTCS in a 48-year-old, detailed history with informed consent taken from his family.

18TH: Case blogged, literature review on possible treatment options explored.

19TH: Reviewed literature related to alcohol withdrawal-induced seizures and altered sensorium.

20TH: Took up a case of Covid pneumonia in a 58-year-old female, detailed history with signed consent was taken from her family.

21ST: Case blogged, the literature reviewed on autoimmune post covid syndromes.

22ND: Updating my knowledge of the interrelation between Diabetes and Covid-19 and how steroids affect them

23RD: Took another COVID case of a woman with a non-healing ulcer and a history of hypertension.

Detailed history and signed consent were obtained.

24TH: Read literature surrounding the causes of non-healing ulcers and treatment modalities

25TH: Blogged the case of non-healing ulcer, read about the possible benefits of platelet-rich plasma in burns patients.

26TH: Went through the bimonthly GM assignment, and tried finding relevant scientific articles related to the cases mentioned.

27TH: Went through questions posed by classmates in the monthly GM assignment, and provided answers based on my comprehension of the cases.

28TH: Studied a case of liver abscess in a chronic alcoholic and tried to find any links between toddy consumption and amoebic liver abscess. Worked on the GM bimonthly assessment.

29TH: Studied a case of an SOB in a patient with cardiogenic shock post-MI that was relieved by the administration of i.v fluids and tried to establish a relation between the two. Worked on the GM bimonthly assessment.

30TH: Went through questions posed by classmates in the monthly GM assignment, and provided answers based on my comprehension of the cases. Worked on the monthly master chart for covid patients in our hospital.