Bimonthly assignment- May

 

1) Pulmonology (10 Marks) 

 

A) Link to patient details:

 

 

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 in this patient in terms of an event timeline:

• 20 years ago: the patient had an episode of SOB (grade II) during the month of January while working on the paddy fields which decreased on taking inhalers.  It eepeated 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: patient was treated for anemia with iron injections 
• 1 month ago: patient started experiencing generalized weakness. 
• 30 days ago:  patient had her latest episode of SOB.
• 20 days ago: patient had an HRCT done due to suspicion of COVID.
• 15 days ago: patient  developed pedal edema.
• 15 days ago: patient developed facial puffiness. 
• 2 days ago: patient had reduced urine output .

The anatomical localization of the disease is at the lungs

The primary aetiology of her problem is COPD that has led to right heart failure. The COPD is most probably a consequence of using an 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?

Pharmacological interventions:

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 su8bunit.
• Indication: Community acquired pneumonia, tonsillitis, acute exacerbation of COPD, PID
• Efficacy: effective against staphylococci, streptococcus and moroxella along with many other gram8 positive and negative bacteria

3. Lasix

• 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. Ipravent2

• 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, beri beri

Non-Pharmacological interventions:

1. O2 supplementation

• MOA: Acts by increasing alveolar oxygen partial pressure
• Indications: decreased SPO2

2.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?

• Allergens: like pollen, wood smoke (choola)
• Respiratory infections: responsible for half of all acute exacerbations. Commonly due to H. Influenzae, S. Pneumoniae, Moraxella catarrhalis.
• Air pollution 
• Toxins

 

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

Yes, ATT could have affected her symptoms.

According to the history the patient started d2eveloping pedal edema and facial puffiness a few days after starting ATT. As these both are signs of re2nal 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 hypochloremia and hyponatremia.

hypochloraemia  could have been a consequence of  heart failure in addition to her treatment with diuretics such as Lasix (furosemide).  

     The hyponatremia can be a consequence of AKI. In AKI there is a loss of renal function thus compromising its ability to reabsorb sodium leading to excess urinary sodium loss. Hence the hyponatremia.

     

 

 

2) Neurology (10 Marks) 

 

A) Link to patient details:

 

h2ttps://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

 

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?

Ev2olution of the symptomatology:

20029 (12 years ago): the patient Started drinking alcohol

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

2020 (1 year ago): the patient had an episode of seizures (most likely GTCS)

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

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

Tuesday, May 11, 2021: the patient food intake decreased. He Started talking and laughing to himself. He was unable to lift himself off the bed, help was required. 

  He was Conscious, but non coherent. Disoriented to time, person, place. He was taken to an RMP the same day- is prescribed IV fluids and asked to visit a hospital.

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

Anatomical localisation of problem:  the brain -hippocampus and frontal lobe.

 

Primary etiology of patient's problem: Chronic Alcoholism

 

 

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

MOA: Thiamine is necessary to provide energy to the CNS, helps in 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

2. Inj. Lorazepam

MOA: Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell.

Indication: Used to sedate patient

Efficacy: High efficacy

3. T. Pregabalin 75mg/PO/ BD

MOA: Acts by releasing GABA

Indications: in seizures

Efficacy: Newer antiepileptic, good efficacy with fewer side effects

4. Inj. HAI S.C.- premeal

MOA: Short- acting insulin

Indications: Diabetes Mellitus

Efficacy: Effective for short periods of time

5. Lactulose 30ml/PO/BD

Given for same reason as Ringer's lactate

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

7. Syp Potchlor 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 were absent during withdrawal earlier? What could be a possible cause for this?

A possible cause for this is due to a phenomenon known as kindling. In kindling, repeated attempted alcohol detoxification leads to an 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 leads 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).

 

4) What is the reason for giving thiamine in 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 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?

The most probable reason for kidney injury in this patient  is generalised dehydration. 

 

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

Probable causes of normocytic anaemia are:

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

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

·          Loss of blood through chronic foot ulcer

 

 

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

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

 

 

 

B) Link to patient details:

 

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?

Evolution of the symptomatology

Since 1991(30 years ago): Patient has been drinking alcohol, 90-180ml per day

May 13, 2021: he Felt giddy, which subsided after a while. He had one episode of vomiting

May 13-16: patient stopped consumption of alcohol

May 16, 2021: he Consumed alcohol again.

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

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

Anatomical location: Infarct in the right inferior cerebellar hemisphere

Primary etiology: Cerebellar infarction, most probable cause: Primary HTN

 

 

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.       Inj Zofer 4 mg IV/TID

MOA: 5-HT receptor antagonist

Indication: Ondansetron, used as an anti emetic

Efficacy: Effective

 

2.       Tab Ecosprin 75 mg PO/OD

MOA: Aspirin, Cyclo-oxygenase inhibitor

Indication: To prevent strokes

Efficacy: Used as a preventive measure

 

3.       Tab Atorvostatin 40 mg PO/HS

MOA: Statin, HMG CoA reductase inhibitor

 

 

 

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

Yes, as 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 patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic 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 ischaemia, hence causing ischaemic stroke.

 

 

 

 

 

C) Link to patient details:

 

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?

Evolution of the symptomatology

2011, 10 years ago: The patient had One episode of quadriplegic paralysis

October 2020: The patient developed bilateral pedal edema, pitting type

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

May 11, 2021: The patient complained of palpitations, sudden in onset, associated with dyspnoea (grade 3), Chest pain with chest heaviness.

Anatomical localisation: Skeletal muscle, Neuromuscular junction

Primary etiology: Hypokalemia (decreased serum potassium)

 

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

the reasons for recurrence of hypokalemia is Possibly inherited or idiopathic causes for hypokalemia.

Risk factors of hypokalemia:

• Female
• Medications (diuretics)
• Heart failure
• Hypertension
• low BMI
• Alcoholism
• Diarhhoea/ severe vomiting
• Cushing syndrome

 

 

3) What are the changes seen in ECG in 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. 

 

 

 

D) Link to patient details:

 

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

 

 

QUESTIONS:

 

 

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

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

 

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

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.

 

 

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. 

 

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

The reason for his IC bleed may be:

• 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) 

Yes, Alcoholism contribute to bleeding diatheses

 

 

F) Link to patient details:

 

 

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 accident 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.

 

2.What are warning signs of CVA?

 

3.What is the drug rationale in CVA?

• Mannitol, osmotic agent- to decrease cerebral edema, increase cerebral perfusion
• Aspirin, antiplatelet- prevention of stroke again, to prevent other thrombotic events
• 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 ischaemia, hence causing a stroke.

 

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

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

 

G) Link to patient details:

 

 

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

 

 

__*Questions*_

 

1)What is myelopathy hand?

It is characterised by loss of adduction and extension of the ulnar 2-3 fingers. Inability to rapidly grip and release with these fingers is also seen. There is weakness and wasting of the muscles but no sensory involvement.

This is due to pyramidal tract involvement. It is seen in various cervical spine disorders with spinal cord involvement. 

 

 

 

2)What is finger escape ?

Finger escape is elicited by asking the patient to hold their fingers in extension and abduction. The little and ring fingers slowly fall into flexion and adduction within 30 seconds. This happens because of poorly innervated palmar interosseous muscle between the fourth and fifth metacarpals susceptible in myelopathy.

It is a sign of cervical spinal cord problems like cervical myelopathy.

 

 

3)What is Hoffman’s reflex?

Hoffman’s reflex is performed by loosely holding the middle finger and flicking the fingernail downward, allowing the middle finger to flick upward reflexively. 

Positive response: 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.

 

 

H) Link to patient details:

 

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

 

  

Possible questions: 

 

              

1)      What can be the cause of her condition ?

·         The patient was suffering from acute cortical vein thrombosis which led to a haemorrhagic venous infarction. In cortical vein thrombosis due to the close contact of cortical veins to the cerebral cortex, local alterations are of the blood–brain barrier are produced which also trigger seizures.

·         In addition, occlusion of the superior sagittal sinus and cortical veins, which drain venous blood from motor and sensory cortices could increase the risk of seizures due to damage to the motor cortex.

·         If haemorrhage occurs, focal cortical irritation caused by blood metabolites could also predispose acute seizures.

                            

 

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

Risk factors for cortical vein thrombosis in adults:

• Clotting disorders such  as: antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency
• Pregnancy
• Cancer
• Obesity 
• Collagen vascular disorders like : wagner's granulomatosis, behecet syndrome .
• Intracranial hypotension.
• Inflammatory bowel diseases like crohn's disease and ulcerative colitis.

 

 

3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously  why?    

Seizures after CVA tend to be of two types:

·         Early

·         Late.

Early seizures are usually seen within 24 days of the incident and the late seizures occur 1-2 weeks after the incident. The patient’s seizures on 1/5/21 can be case of early onset seizures and on 10/5/21 can be late onset.

 

                      

             

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

·         Clexane (Enoxaparin) an anticoagulant

·         mannitol (to decrease the intracranial pressure)

 

 

3) Cardiology (10 Marks) 

 

A) Link to patient details:

 

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

 

 

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

 

2.Why haven't we done pericardiocenetis in this pateint?      

Pericardiocentesis was not done in the patient as he was hemodynamically stable and his pericardial effusion was improving with medical treatment. It had come down to 1.9 cm from an initial value of 2.4 cm

  

 

             

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

• Advanced age
• Diabetes 
• Hypertension 
• Smoking
• Alcohol consumption 
• Anaemia
• Renal disorders

 

 

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

·         Diastolic dysfunction could be the reason for the hypotension.

·         Diastolic dysfunction can lead to hypovolemia which in turn can lead to  hypotension.

·         The patient was also on Lasix which can again lead to hypovolemia.

·         Anaemia can also be a contributing factor to the hypotension.                 

 

 

B) Link to patient details:

 

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 risk factors for heart failure in this patient include:

• Advanced age
• Diabetes 
• Alcohol consumption 
• Anemia
• Renal disorders
• Obesity

 

 

 

2.what is the reason for anaemia in this case?

·         Erythropoietin (hormone responsible for erythropoiesis) is produced by interstitial fibroblasts  of kidney.

·         In kidney diseases like CKD, the erythropoietin production decreases due to damage to the kidneys thus leading to anaemia.

·         Another proposed mechanism for anaemia in CKD is the inhibition of erythropoiesis by uremic induced inhibitors.

 

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

Bleb which were formed on the toe could be due to the tight fitting of the footwear. As they fit too tight, they rub against the skin. This causes friction as a result of which fluid builds up underneath the upper layer of skin. This is often seen in patients with long standing diabetes due to loss of sensation as a result of peripheral neuropathy.

 Peripheral neuropathy caused by diabetes could be a contributing factor. In addition diabetes causes peripheral arterial disease that leads to decreased peripheral blood flow which delays the healing. Diabetes is a common cause for non-healing ulcers.

 

 

 

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

The patient’s obesity is likely to have caused insulin resistance (stage 1).

This later developed into frank diabetes. (stage 3).

As the patient shows signs of vascular complications such as diabetic retinopathy, nephropathy and peripheral neuropathy which are complications of diabetes, it could be said that the patient has stage 4 diabetes mellitus. 

 

 

 

C) Link to patient details:

 

 

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

 

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:

• 2-3 years ago: patient had episodic facial puffiness 
• 1 year ago: patient developed grade 2 SOB
• 1 year ago: patient was diagnosed with hypertension
• 2 days before admission: patient’s SOB grade 2 progressed to grade 4
• 2 days before admission: patient’s urine output decreased.

    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?

Pharmacological interventions:

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: heatr 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, beri beri.

 

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

Pathogenesis of cardio renal syndrome:

The patient has type 4 cardio renal syndrome.

 

 

6)      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.

 

 

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

The patient is asked to get these test for review to ensure that the coagulatory parameters remain normal, if not, there is a need to modify the treatment in order to bring them to normal levels.

 

 

D) Link to patient details:

 

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.

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

·         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/

 

 

3) 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

 

 

 

4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on 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.

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

·         Overtreatment continues to be a major contributor to excessive healthcare spending. When there is 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.

 

 

 

E) Link to patient details:

 

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 of the problem: damage to the myocardial muscle(heart) due to obstruction in the coronary artery.

·         Primary aetiology of patient’s problem: 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.

 

 

F) Link to patient details:

 

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

 

1. How did the patient get  relieved from his shortness of breath after i.v fluids administration by 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 of 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 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/

 

 

 

4) Gastroenterology (& Pulmonology) 10 Marks

 

A) Link to patient details:

 

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 of the problem:  Pancreas

·         Primary aetiology of the patient’s problem:  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

 

B) Link to patient details:

 

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

 

 

1)      What is causing the patient's dyspnea? 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 hyperglycemia.

·         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 and to maintain volume status. (IVF) 

pain management using narcotic agents(tramadol).

ZOFER  is given which is an anti-emetic.

 

 

 

C) Link to patient details:

 

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

 

Possible 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 mimic 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

 

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/

 

5) Nephrology (and Urology) 10 Marks 

 

A) Link to patient details:

 

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

 

1. What could be the reason for his SOB ?

The most possible reason for his SOB is 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 ?

Intermittent episodes of  drowsiness are due to hyponatremia.

 

3. Why did he complaint 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:

·         Electolyte abnormalities

·         Pain during micturition

·         UTI

·         Urinary bladder thickening

 

 

 

 

6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)  10 Marks 

 

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 tracheo esophageal fistula?

clinical history and physical findings are characteristic of tracheo esophageal fistula are:

·         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

 

 

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

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

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

 

 

7) Infectious disease and Hepatology:

 

Link to patient details:

 

 

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

 

 

 

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

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 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 liver abscess ?

Indications for ultrasound guided aspiration of liver abscess are:

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

 

 

 

 

 

B) Link to patient details:

 

 

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

 

QUESTIONS:

 

 

1) Cause of liver abcess in this patient ?

Toddy connsumption

 

 

2) How do you approach this patient ?

Medical management: 

• Antibiotics: Metronidazole, paromomycin, diloxanide furoate+broad spectrum antibiotics (for secondary infections/ if it's a pyogenic abscess) 
• Analgesics: NSAIDs, opioid analgesics (in cases of severe pain)
• Antipyretics: Paracetamol
• 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 abcess? 

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.

 

 

 

8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks 

 

A) Link to patient details:

 

 

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 etiology 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 periorital edema. 04/05/21: he had altered sensorium and had weakness in right upper and lower limb.

·         Anatomical localization of the problem: Orbit, nose, oral cavity, pancreas, left frontal and temporal lobe

·         Primary aetiology: 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) is the drug of choice to treat mucormycosis.

·         Adjunctive therapy with 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 of time? 

Mucormycosis is an opportunistic fungal infection. That means it infects people who have a weak immune system, that includes diabetic patients, patients taking cortico-steroids 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 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 usage of steroid for a long time. All such reasons, have led to the sudden increase in the incidence of mucormycosis in india.

 

9) Infectious Disease (Covid 19)

 

As  these patients are currently taking up more than 50% of our time we decided to make a separate log link here:

 

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

 

for this question that contains details of many of our covid 19 patients documented over this month and we would like you to:

 

1) Sort out these detailed patient case report logs into a single web page as a master chart 

 

2) In the master chart classify the patient case report logs into mild, moderate severe and 

 

3) indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements 

 

4) Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension etc). 

 

 https://docs.google.com/spreadsheets/d/e/2PACX-1vQuWFPoQm48IiBs1aDOGHPMosE9sylv2WdixecZa7xbmudlxrGMxk1O_1fgKpNxBbNPZLpIy37oQPcy/pubhtml

 

1) Covid 19 with co morbidity (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) 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).

 

CASE 9-2: COVID-19 SEVERE

 

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

 

QUESTIONS:

 

1) Since patient didn't show any previous characteristic diabetes signs, did the Covid-19 infection aggravate any underlying condition and cause the 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: [6]

 

 

 

 

 

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

Yes, with DM or hypergycemia 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, hyperglycaemia 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 increasing severity of COVID-19 [7]. Moreover, D- dimer levels would be helpful in fast diagnosis and prevention of thrombotic complications.

 

 

 

 

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 an increased inflammation and immunological dysfunction in COVID, elevated ESR is most likely dur 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 harms of hospitalization?

Hospitalisation was due to Grade 3 Shortness of Breath (SOB), and 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 labourers, cannot afford to home isolate as they need to earn on a daily basis to keep their family going

Harms of hospitalisation-

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 hospitalisation

         

 

 

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 coma in this patient?

The reason for 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 make a diagnosis of hypokalemic periodic paralysis based on the fact that the patient had generalised 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 include

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

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

 

2. what is the cause of death in this patient?

The cause of death in this patients 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.

 

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

7) A 67 year old lady in the ICU with COVID induced Viral Pneumonia .

 

 

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

Q1. What is the grade of pneumonia in her?

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

Q2. What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?

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

Q3. What all could be the factors that led to psychosis in her ?

A. 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

Q4. In what ways shall the two drugs prescribed to her for psychosis help ?

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

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

Q5. What all are the other means to manage such a case of psychosis?

A. 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.

 

 

 

 

Q6. What all should the patient and their attendants be careful about ( w.r.t. COVID )after the patient is discharged ?

A. 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.

Q7. What are the chances that this patient may go into long covid given that her "D Dimer" didn't come down during discharge? 

A. 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.

 

 

8) 35YR/M WITH VIRAL PNEUMONIA SECONDARY TO COVID 19 INFECTION

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

 

Q1. Can psoriasis be a risk factor for severe form of COVID?

A. 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.

Q2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?

A. 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.

Q3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?

A. 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.

9) 45 year old female with viral pneumonia secondary to Covid-19

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

Q1. What is the type of DM the patient has developed ?(is it the incidental finding of type 2 DM or virus induced type 1DM)? 

A.  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 ofthe 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.

Q2. Could it be steroid induced Diabetes in this patient?

A. 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.

 

10) A little difference that altered the entire covid recovery game: a report of two patients with focus on imaging findings.

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

Q1. What are the known factors driving early recovery in covid?

A. The following factors can lay a role:

• Younger age ggroup
• shorter duration of fever 
• No diabetes
• PaO2/FiO2 levels
• No comorbidities

 

11) Viral pneumonia secondary to COVID of a  denovo Diabetes Mellitus

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

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? 

A. 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 tendtendvbe better diagnosis.

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.

 

Q2. Why couldn't the treating team start her on oral hypoglycemics earlier?

A.      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.

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/

13) Severe covid with first diabetes 

 

Link to Case report log :

 

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

 

 

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.

 

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)

 

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

 

 

 

 

17) Covid 19 with hypertension comorbidity 

 

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

 

 

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 assocatied with a weaker immune system and is seen in older patients which show 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 permeability of microvascular circulation which lead to pleural effusion(exudative type)

 

18) Covid 19 with mild hypoalbuminemia 

 

 

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 simulataneous 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.

 

2.       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 increase in work load of the heart. To compensate this demand, the ventricles undergo remodelling leading to cardiomegaly.

 

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

·         Chicken pox

·         Shingles

·         Pytriasis

 

4.       Why is there 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.

 

20) Covid 19 with first time diabetes 

 

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 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 diabetic patient has shown a increase in death rate as it further decreases the immunity of the patient and make them prone to other opportunistic infections like mucormycosis leadth to inceased 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 viscocity 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 effect on the out come of Covid infection?If yes,how?

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

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

Reduced resistance to COVID-19 promotes progression of disease and leading to wrose prognosis

 

21) Severe Covid with Diabetes 

 

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 a 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 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. In a patient who has a history of CVA are mostly old and have other co-morbidities which leads to severe course of the disease as well as poor prognosis.

 

23) Covid 19 with multiple comorbidities:

 

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

 

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 asthama

 

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

·         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 diabetes, there is a increase in blood flow to the kidneys, which strains the glomeruli and lessenstheir ability to filter blood. High levels of glucose in the blood leads to accumulation of extra material in glomeruli. It increases the stress of glomeruli inturn leading to gradual and progressive scarring. Eventually leads to the development of CKD.