MEDICINE CASE BASED LEARNING
I have been given the following cases to solve in an attmept to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and coem up with a treatment plan.
1) Pulmonology
2)NEUROLOGY
Answer:
The following is the event timeline of symptom occurrences
in the patient:
An episode of seizure (GTCS) one year ago
Latest episode of Seizure 4 months ago associated with
restlessness, sweating, and tremors following cessation of alcohol
9 days ago, patient developed Altered mental state with discontinuous
spatial and temporal orientation, loss of appetite, weakness
After admission, tremors, sleep disturbances, sweating
Involuntary rolling of eyes, tongue biting, frothing, loss
of consciousness
Anatomical localisation:
Wernicke’s encephalopathy is normally localised to frontal
lobe, thalamus and hypothalamus.
Uremic encephalopathy is usually confined to basal ganglia,
thalamus and midbrain
The possible etiological factors could be the following:
Alcohol use disorder in addition to poor appetite leading to
Vit. B1 (Thiamine) deficiency
Uremia could be secondary to prerenal acute kidney injury
Question 2:
What are mechanism of action, indication and efficacy over
placebo of each of the pharmacological and non pharmacological interventions
used for this patient?
Answer:
The pharmacological and non pharmacological intervention
provided include the following:
Thiamine
MOA: Replenishment of the thiamine lost reserves of Thiamine
Indication: Chronic Alcoholism could be a potential cause of
Thiamine deficiency
Efficacy: For the treatment of acute Wernicke’s
encephalopathy, the case series given below demonstrates that IV thiamine
appears efficacious and safe for use
Reference link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354137/
Lorazepam
MOA: Acts on GABA-A receptors produces an increase in the
frequency of opening of the chloride ion channel
Indication: Alcohol withdrawal syndrome and Seizure activity
Efficacy: Oral benzodiazepines are the best studied and most
effective drugs for preventing a severe alcohol withdrawal syndrome
Reference link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606320/
Pregabalin
MOA: Crosses the BBB and enhances the release of GABA but
does not act as an agonist on the GABA-a receptor
Indications: Alcohol withdrawal syndrome and Seizure
activity
Efficacy: Separate analyses of the pregabalin and the
placebo group showed a significant reduction in diazepam use from Day 2 to 6
(pregabalin: Z = −2.842, P = 0.004; placebo: Z = −2.916, P = 0.004).
Reference link:
https://academic.oup.com/alcalc/article/47/2/149/187301
Question 3:
Why have neurological symptoms appeared this time, that were
absent during withdrawal earlier? What could be a possible cause for this?
Answer:
It is possible that the patient developed higher dependence
with time when compared his previous attempts to cease alcohol consumption.
Question 4:
What is the reason for giving thiamine in this patient?
Answer:
As the patient is a chronic alcoholic, there is a
possibility that he has developed Thiamine deficiency. If the thiamine
deficiency is left untreated, these complications can result in irreversible
damage to several parts of the CNS and develop Wernike’s Encephalopathy. Hence
in order to prevent any irreversible damage, thiamine has been administered.
Question 5:
What is the probable reason for kidney injury in this
patient?
Answer:
Elevated levels of urea and creatinine are suggestive of
Prerenal Azotemia being the most likely cause of kidney injury in this patient.
This can be a result of decreased blood flow to the kidneys possibly due to
dehydration secondary to Alcoholism.
Question 6:
What is the probable cause for the normocytic anemia?
Answer:
The possible causes of anemia can be the following:
Chronic alcohol dependence causing decreased erythropoiesis
as there is a direct toxic effect of alcohol on the bone marrow
Anemia can be secondary to poor nutrition and malabsorption
syndrome
Alcoholic gastritis that could have caused a hemorrhage in
the stomach leading to loss of blood
Possibility of liver cirrhosis that could have caused
sequestration of RBCs in spleen
Question 7:
Could chronic alcoholism have aggravated the foot ulcer
formation? If yes, how and why?
Answer:
Alcoholic polyneuropathy could be the most probable cause of
ulcer formation. The patient is also a known case of diabetes since two years.
So it is also likely for the uncontrolled diabetes to have caused diabetic
neuropathy and lead to diabetic foot ulcer.
The minor incidents of falls could have caused concussions in the brain and hence Ataxia
Alcohol consumption could also have caused cerebellar dysfunction and resulted in ataxia
Question 2:
What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Answer:
The reasons for IC bleed could be the following:
The patient has history of multiple episodes of fall which had lead to minor head injuries
Cirrhosis of liver, leading to sequestration of platelets causing thrompocytopenia and hence increased intracranial bleeding tendencies.
• Cortical
vein thrombosis.
2) What are the risk factors for cortical vein thrombosis?
• Clotting
disorders
• Sickle
cell anemia
• Chronic
hemolytic anemia
• Beta-thalassemia
major
• Heart
disease — either congenital or acquired .
• Iron
deficiency
• Dehydration
• Head
injury
• Pregnancy
• Perperium
• Oral
Contraceptive pills
3)There was seizure free period in between but again sudden
episode of GTCS why?resolved spontaneously
why?
• There may
be some edema that was not resolved and was excitable,that might have lead to
further seizure reccurence.
5) What drug
was used in suspicion of cortical venous sinus thrombosis?
• Clexane
was used which is an anticoagulant.
3)Cardiology
B) Link to patient details:
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html.
Questions:
1. 1. What are the possible causes for heart failure in this patient?
·
As the patient is
known case of hypertension since 19 years it is a major risk factor for heart
failure it
·
Sclerotic aortic
valve need more work done by the left ventricle which can lead to dialated left
ventricle and heart failure
·
Diabetes is a
risk factor for heart failure as it leads to hypertension and elevated lipid
levels both of which may cause atherosclerosis which is a cause of heart
failure
·
The chronic
anemia present in the patient may be a risk factor as total volume of blood is
less and heart needs to work harder to supply to all organs
·
The chronic
kidney disease is one of the causes of heart failure as it releases more renin
to increase blood supply to kidneys it leads to more work load on heart
resulting in heart failure
2.
What is the
reason for anemia in this case?
·
Due to chronic
kidney disease, the kidneys fail to produce erythropoietin that is needed for
rbc production this is the reason for chronic anemia in this case
3.
What is the
reason for blebs and nonhealing ulcer in legs of Patient?
·
The patient
already has diabetes which is risk factor for non healing ulcer and due to
heart failure ,the rate of perfusion and oxygenation to extremities is reduced and
can delay healing
4.
What sequence of
stages of diabetes has been noted in this patient?
·
Diagnosed with
type 2 diabetes 30 years ago
·
Diabetic
retinopathy causing blurring of vision since 4 years (vascular complication)
·
Diabetic nephropathy
·
Reference :
https://www.kidneyfund.org/kidney-disease/chronic-kidney-disease-ckd/complications/heart-disease/
D) Link to patient details:
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?
· The following is the event timeline of symptoms occurrences
in the patient:
· She had heartburn like episodes which subsided without
medication since 1year
· She was diagnosed with tuberculosis 7 months ago for
which she has completed the course of medication
· She was diagnosed with diabetes 12 years back and with
hypertension 6 months back
· She had the first episode of SOB half an hour ago
· ECG taken then upon admission showed NSTEMI(coronary
syndrome) and she was given TAB
MET XL 25 MG/STAT.
· She was advised to get PCI but she didn’t get it and symptoms subsided and she is doing fine now
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
The pharmacological and non pharmacological interventions
provided include:
· TAB
MET XL 25MG/STAT (Metoprolol)
MOA:by blocking beta-1-adrenergic
receptors on the cardiac cells
Indication : ECG was
suggestive of NSTEMI
Efficacy : The use of early β-blocker therapy in
acute MI reduces the risks of reinfarction and ventricular fibrillation, but
increases the risk of cardiogenic shock, especially during the first day or so
after admission.
· PCI
MOA
: PCI is a non surgical minimally invasive technique in which the balloon
catheter widens the coronary artery and a stent is placedtwith the help of
angiography
Indication
: NSTEMI
Efficacy : in immediate invasive
strategy (<2hours) indicated in very-high-risk NSTEMI criteria, immediate
coronary angiography along with PCI is effective
Reference: https://academic.oup.com/eurheartjsupp/article/20/suppl_B/B10/4944485
3)
What are the indications and contraindications for PCI?
Clinical Indications and
Contraindications to PCI
Indications
- Acute ST elevation myocardial
infarction (STEMI)
- Non ST elevation acute coronary
syndrome
- Stable angina
- Anginal equivalent (eg,
dyspnea, arrhythmia, dizziness/syncope)
- Asymptomatic or mildly
symptomatic patients with objective evidence of a moderate to large area
of viable myocardium or moderate to severe ischemia on noninvasive testing
Contraindications
- Significant comorbidities
(relative contraindication)
Angiographic Indications and
Contraindications to PCI
Indications
- Hemodynamically significant
lesion in a vessel serving viable myocardium (vessel diameter >1.5 mm)
Relative contraindications
- Left main stenosis in a patient
who is a surgical candidate
- Diffusely diseased
small-caliber artery or vein graft
- Other coronary anatomy not
amenable to percutaneous intervention
Reference : https://medicalcriteria.com/web/carpci/
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?
· There are often risks associated with PCI like blood
clots, renarrowing of the coronary artery, bleeding from the site of
catheterization .We may push the patient into these risks when the procedure is
performed in patients who may not need it or when it can be managed by
medication .
· Harms of overtretment are psychological stressors,
morbidity, unnecessary surgical complications as seen after small renal masses
resection surgeries
· Research on overtesing and overtretment is important
because there are downfalls to overtesing and overtretment .
· Huge amount of healthcare money is wasted on
unnecessary treatment and testing and more testing and treatment is not linked
to better outcome and may become worse sometimes
Reference
:
https://onlinelibrary.wiley.com/doi/full/10.1111/acem.12820
https://www.mayoclinic.org/tests-procedures/coronary-angioplasty/about/pac-20384761
2. What is the rationale of using torsemide in this patient?
• Torsemide
was used because patient had cardiogenic pulmonary edema which caused shortness
of breath in him.
• Torsemide
decreases fluid volume(pulmonary oedema) as it is a diuretic .
• It blocks
the sodium pottasium channels in ascending loop of henle and thus blocking
their absorption leading to exrcretion in urine.
3. Was the rationale for administration of ceftriaxone? Was
it prophylactic or for the treatment of UTI
• May be
prophylactic use because the patient did not have UTI symptoms like urgency or
dysuria.
4) Gastroenterology & Pulmonology
5) Nephrology and Urology
During TURP, the wide plexus of venous sinuses is often opened and the absorption of the irrigation fluid causes a group of symptoms and findings that is called TURP syndrome.2 Absorption of the irrigation fluid (2000 ml or more) may lead to TURP syndrome which causes headaches, anxiety, confusion, dyspnoea, arrhythmia, hypotension and seizures and can be fatal if not treated. The symptoms of TURP are generally caused by an excessive fluid load in circulation
2. why does he have intermittent episodes of drowsiness ? It might be due to uremic encephalopathy
3. why does he complain of fleshy mass like thing passing in the urine?
I It might be the blood clot or scab falling off the prostate during healing after the turp surgery
4.what are the complications of
turp he may have had?
Urinary tract infection
Passing of blood clots in urine
TURP syndrome
References :https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4543890/
https://www.ncbi.nlm.nih.gov/books/NBK564327/
https://www.nhs.uk/conditions/transurethral-resection-of-the-prostate-turp/recovery/
B) Link to patient
details:
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 ?
The child
might have had attention deficient hyperactive disorder (ADHD) because of which
he may be hyperactive and due to his less attention span he may be impulsive
and may not be able to interact with others much so he may not have much social
etiquettes
2. Why doesn't the child have the excessive urge of urination at night time?
The child may be having psychosomatic urge to
urinate during the day but this will not
be present during sleep as he will not be conscious
3. How would you want to manage the patient
to relieve him of his symptoms?
Urinating on
schedule and gradually lengthening the time between bathroom visits
Medication. Drugs that
relax bladder like botox injection
Anti anxiety drugs
Nerve stimulation. This includes some of the latest treatment options for OAB. They
sometimes may help when there is
no improvement with medications
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
• Cough on
taking food and liquid.
• Difficulty
in swallowing.
• Weight
loss of 10kg.
Physical findings suggestive of tracheooesophageal fistula:
2) What are the chances of this patient developing immune
reconstitution inflammatory syndrome? Can we prevent it?
The suppression of CD4 T cells by HIV causes a decrease in
the body's normal response to certain infection.
If the CD4 count
rapidly increases (due to effective treatment of HIV, or removal of other
causes of immunosuppression), a sudden increase in the inflammatory response
produces nonspecific symptoms such as fever, and in some cases a worsening of
damage to the infected tissue.
There are two common IRIS scenarios. The first is the
“unmasking” of an occult opportunistic infection. The second is the
“paradoxical” symptomatic relapse of a prior infection despite microbiologic
treatment success. Often in paradoxical IRIS, microbiologic cultures are
sterile. In either scenario, there is hypothesized reconstitution of
antigen-specific T cell-mediated immunity with activation of the immune system
following HIV therapy against persisting antigen, whether present as intact
organisms, dead organisms, or debris.
To prevent IRIS , ART treatment is given before CD4 cells
count go down below 100cells/ul.
We should prevent advanced immunosuppression.
Reference :
7) Infectious disease and Hepatology:
A. In this case, LOCALLY-BREWED ALCOHOL can be the possible
cause of liver abscess because alcoholism, mainly consuming locally prepared
alcohol plays a major role as a predisposing factor for the formation of liver
abscesses that is both amoebic as well as pyogenic liver abscess because of the
adverse effects of alcohol over the Liver.
Following alcoholism, poor economic status & malnutrition also plays
a vital role as predisposing factors in the formation of liver abscess. Among
alcoholism also, consuming locally prepared alcohol plays a vital role, but the
reason is still been unknown.
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic
patient ? ( since 30 years - 1 bottle per day)
A. 1.] Factors influencing the association could be related
to the:
Pathogen
Contents of beverages
Status of the liver
Immunity of the host.
Large infective dose
of Entamoeba histolytica or Other bacterial pathogens ingested with the
unhygienically brewed beverage.
Nutritional status of
the population
Poor sanitation
Alcohol-induced
hepatic dysfunction
Possible suppression
of amoebistatic immune mechanisms by substances in the beverages could also be attributed in
the mechanism.
2.] Mechanisms responsible:
Hepatic damage by alcohol,
Lowered body resistance and
Suppression of liver function due to poor nutritional status
of habitual consumers of alcohol,
Increased presence of amoebae in the liquor prepared locally
with poor regard to aseptic procedures, and
Depression of immune mechanisms in chronic alcoholics.
3. Is liver abscess more common in right lobe ?
A. Liver abscess is more common in right lobe because of
more blood supply to the right lobe relatively. Due to this fact pathogens are
carried in increased proportions to the right
lobe.
4.What are the indications for ultrasound guided aspiration
of liver abscess ?
A. INDICATIONS OF
LIVER ABCESS DRAINAGE:
1) If the abcess is large ( 5cm or more) because it has more
chances to rupture.
2) If the abcess is present in left lobe as it may increase
the chance of peritoneal leak and pericardial leak.
3) If the abcess is not responding to the drugs for 7 or
more days
A) Most amoebic
infections are caused by Entamoeba histolytica. The pyogenic abscesses are
usually polymicrobial, but some organisms are seen more commonly in them, such
as E.coli, Klebsiella, Streptococcus, Staphylococcus, and anaerobes.
While the
incidence is low, it is essential to understand the severity of these abscesses because of the high
mortality risk in untreated patients.
If the cause is infectious, the majority of liver abscesses
can be classified into bacterial (including amebic) and parasitic sources
(including hydatiform cyst).
The right
lobe is more commonly affected lobe.
2) How do you approach this patient ?
A.Treatment along with rationale:
INJ. ZOSTUM 1.5mg IV (twice daily):
Zostum is a combination of drugs - SULBACTUM (pencillin) & CEFOPERAZONE(cephalosporin) [Antibiotic]: It
is used here to treat if any bacterial cause ( since we can’t take the risk
relying on only anti amoebic therapy)
INJ. METROGYL 500mg IV TID
Metrogyl has the drug called METRONIDAZOLE [Antibiotic]: For
amoebic cause
INJ. OPTINEURIN 1amp in 100ml NS IV OD:
Optineurin is a multivitamin drug {A combination of B1,B2,
B3, B5,B6, B12 } given here as a supplement
TAB. ULTRACET 1/2 QID:
Ultracet is a combination of drugs - TRAMADOL(opiod
analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and
fever
TAB. DOLO 650mg
sos, given for fever and pain
* Here ; due to medical therapy his symptoms subsided and
clearly we can see it in usg reports ( liquefaction has occured) meaning abcess
responded to our medical therapy.
* We donot aspirate the pus since it is self resolving and
aspiration is associated with several other complications.
3) Why do we treat here ; both amoebic and pyogenic liver
abscess?
A. Empirical antibiotic coverage is essential when the
organism is unknown. The antibiotics should cover Enterobacteriaceae,
anaerobes, streptococci, enterococci, and Entamoeba histolytica. Such
antibiotic regimens include cephalosporins plus metronidazole, Beta-lactam
Beta-Lactamase inhibitor plus metronidazole, or synthetic penicillins plus
aminoglycosides and metronidazole.
Metronidazole should cover Entamoeba histolytica. The
duration of treatment varies but is usually from two to six weeks. After initial
intravenous treatment, the oral route can be used safely in most cases to
complete the course.
4) Is there a way to confirm the definitive diagnosis in
this patient?
A. As the condition subsided with empirical treatment in
this patient, there is no need of a definitive diagnosis in this patient.
But a definitive diagnosis can be achieved if the abscess is
aspirated and sent for culture.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
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:
Day 1-Patient took covid vaccination, on that night patient
had high grade fever assosciated with chills and rigor , relieved on medication
Day 4 – Patient had fever assosciated with chills and rigor
but not relieved by medication.
Day 11- patient complains of generalised oedema, facial
puffiness, periorbital edema.
Day 17- Altered state , facial puffiness, periorbital oedema
and weakness of right upper and lower limb.
• Anatomical
localization of problem:
Frontal and temporal lobe of brain - infarcts
Orbit
Oral cavity : eshcar extending from hard palate to lip
Left nasal cavity
• Primary
etiology of patients problem
Mucormycosis infection causing rhino-orbito-cerebral
mucormycosis.
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?
• Azoles.Itraconazole
is the only marketed azole drug that has in vitro activity against Mucorales.
There are case reports of successful therapy with itraconazole alone .However,
as mentioned above, itraconazole prophylaxis has been described as a risk
factor for breakthrough mucormycosis .
•
3) What are the postulated reasons for a sudden apparent
rise in the incidence of mucormycosis in India at this point of time?
• Covid 19
infection among diabetic patients in whom there is lower immunity.
• Increased
dose of steroid usage and also because of lower availability of remedesivir ,
tocilizumab leading to dependance on steroids for treatment.
• Use of
ordinary water instead of sterile water in humidifiers.
• Prolonged
ICU stay.
9)INFECTIOUS DISEASE(covid 19)
Covid case 1)
Covid 19 with co morbidity (Pulmonology/Rheumatology)
https://nikhilasampathkumar.blogspot.com/2021/05/covid-pneumonia-in-pre-existing-case-of.html
Possible questions:
1) How does
the pre-existing ILD determine the prognosis of this patient?
• Patients
with ILD have diminished pulmonary reserve and impaired gas exchange due injury
to alveolar epithelium.
• Prognosis
of covid19 patients with preexisting ILD is significantly worse than non ILD
patients.
2) Given the
history of autoimmune disease in the patient, how does the administration of
steroids for COVID affect her RA and hypothyroidism?
• Studies
have shown that steroids used for treatment did not worsen the prognosis of
rheumatoid arthritis.
• https://www.health.harvard.edu/blog/does-lupus-or-arthritis-affect-your-prognosis-if-you-get-covid-19-2020110921230#:~:text=There%20was%20some%20good%20news,prognosis%20for%20the%20arthritis%20patients.
• Couldn’t
find studies,how steroids affect hypothroidism.
3) Would this
patient have an increased risk for post covid autoimmune response compared to
patients without a history of autoimmune disease?
• Not sure
about whether this patient has increased risk for post covid autoimmune
response.
4) Why was
she prescribed clexane (enoxaparin
• IL6 is
involved in cytokine storm,enoxaparin has IL6 binding properties thus
preventing cytokine storm.
• Prevention
of infection by decreasing virus cell entry and hence viral load
• Prevention
of activation of coagulation cascade
covid case 2)
Covid 19 with Diabetes
Link to the patient case report log:
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 exact pathology of new onset diabetes in COVID-19 patients is not known, but this could be a possible explanation. Beta cells in the pancreas contain a significant number of so-called ACE2 receptors. These receptors are believed to be where the spike protein from the coronavirus attaches to cells. Beta cells produce insulin. It is theorised that a coronavirus infection, which affects the ACE2 receptors, might also damage beta cells in the pancreas and hence precipitating diabetes.
2) Did the patient's diabetic condition influence the progression of her pneumonia?
Diabetic subjects may have increased susceptibility to pneumonia for several reasons. They are at increased risk of aspiration, hyperglycemia, decreased immunity, impaired lung function, pulmonary microangiopathy, and coexisting morbidity
3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?
D-dimer is a fibrin degradation product, elevated D-dimer levels have been associated with disease severity and mortality trends. Several studies from Wuhan have shown elevated D-dimer in COVID-19 patients is associated with higher mortality.
There is not yet a consensus as to how D-dimer levels should be used for management and/or monitoring of COVID-19 patients. Checking D-dimer on initial presentation in the emergency department, urgent care facility or outpatient clinic is appropriate.
covid case 3)
Covid 19 Severe
Link to the complete case report log:
https://143vibhahegde.blogspot.com/2021/05/covid-in-26-yo-female.html
Questions:
1. Why was this patient given noradrenaline?
The patient following AKI along with the viral infection could have gone under septicemic shock. This would create a severe hypotensive state. To correct this, Noradrenaline was administered.
2. What is the reason behind testing for LDH levels in this patient?
LDH is often used as a marker of tissue breakdown as LDH is abundant in red blood cells and can function as a marker for hemolysis. It can also be used to diagnose renal infarction. So as the patient has both covid infection and renal complications, LDH works as a diagnostic marker.
3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
As biPAP is not intended for full ventilatory support and is contraindicated in the patients who are unable to maintain spontaneous breathing, invasive mechanical ventilation provides more support to these patients. Once the patient starts to recover and maintain spontaneous breathing, he can be shifted onto an NIV.
covid case 4)
Covid 19 Mild
Link to the case report log:
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?
If there is inflammation following a covid infection, then elevated ESR can be a possible cause of it. During an inflammatory process, increased levels of fibrinogen is released into the blood, causing them to stick together and form rouleaux.
2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization?
The patient was probably admitted as it was a long-standing case of Covid and the patient’s dyspnea had progressed to grade 3 with further exaggeration of his other symptoms also.
If the patient had opted for home isolation, then an emergency could not have been taken care of. And as the patient’s condition was deteriorating with each following day, hospital admission was advisable
As the steroidal therapy given for covid could have disrupted his immune system, admission in a hospital makes him more susceptible to the nosocomial infections.
Case 5)
Covid 19 and comorbidity (Altered sensorium, azotemia, hypokalemia)
Link to the case report log:
https://anuragreddy72.blogspot.com/2021/05/case-discussion-on-hypokalemic-periodic.html
Question 1:
What was the reason for coma in this patient?
Answer:
Hypoxic encephalopathy And Viral encephalopathy probably produced the comatose condition of this patient.
Question 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?
Answer:
Hypokalemic periodic paralysis diagnostic tests??
Question 3:
How may covid 19 cause coma?
Answer:
Infarct in the brain could have developed secondary to embolism which could have been the reason for his coma.
It could also have occurred secondary to hypoxic damage due to low O2 saturation which was a result of COVID infection.
covid case 6)
Severe Covid 19 with altered sensorium
Link to the case report log:
https://vijaykumarkasturi.blogspot.com/2021/05/65-years-old-male-with-viral-pneumonia.html
1. What was the cause of his altered sensorium?
The most probable cause of altered sensorium in this patient can be Hypoxic encephalopathy due to severe fall in SpO2 of the patient.
It can also be Viral Encephalopathy post covid-19 infection
Another possibility is the Hyperglycaemic condition that can cause delirium and even coma might develop. But that would need the evidence of diabetic ketoacidosis.
2. What was the cause of death in this patient?
Hypoxic encephalopathy can be the main cause of the Patient’s death after there was ischemic damage done to the neural tissue.
It could also be due to pulmonary thromboembolism due to Covid infectio
CASE 7
Covid 19 Moderate with ICU psychosis
Link to the case report log:
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?
A) Grade of pneumonia in this patient is MODERATE.
2.What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?
A) Ideal day to start steroids doesnt exist, according to my knowledge, as it depends on the serum markers for covid and reccurance of symptoms. Patients are being given steroids starting with a mild dose of 4-8mg if they have even a mild increase of serum markers, so as to prevent the disease from worsening.
3.What all could be the factors that led to psychosis in her ?
A) There are 3 types of ICU psychosis:
hyperactive
hypoactive
mixed type
Factors responsible for ICU psychosis:
age
Presence of any previous psychological illness
acute or chronic illness
renal disease or impairment
diagnosis of sepsis
smoking
acute respiratory distress
copd
absence of daylight exposure
4.In what ways shall the two drugs prescribed to her for psychosis help ?
A) PIRACITAM: Piracetam improves the function of the neurotransmitter acetylcholine via muscarinic cholinergic (ACh) receptors, which are implicated in memory processes. Furthermore, piracetam may have an effect on NMDA glutamate receptors, which are involved with learning and memory processes.
RISPERIDONE: The primary action of risperidone is to decrease dopaminergic and serotonergic pathway activity in the brain, therefore decreasing symptoms of mood disorders. Risperidone has a high binding affinity for serotonergic 5-HT2A receptors when compared to dopaminergic D2 receptors in the brain.
5.What all are the other means to manage such a case of psychosis?
A) Non pharmacogenic treatment:
Early mobilization activities
Timely removal of catheters and physical restraints
Use of eye glasses and magnifying lenses, hearing aids and earwax disimpaction
Early correction of dehydration
Use of a scheduled pain management protocol
Minimization of unnecessary noise/stimuli
Other drugs can be prescribed like:
Haloperidol
Antipsychotics
6.What all should the patient and their attendants be careful about ( w.r.t. COVID) after the patient is discharged ?
A) As the patient is in the geriatric age group, gaurdians should take all the precautionary measures prescribed by the doctors like:
wearing a mask when near them
sanitising all the household items
maintaining personal hygiene
regular drug administration as prescribed by the physician
frequent monitoring of SpO2 levels.
CASE8)
Covid 19 Moderate
Link to the complete case report log
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?
a) Treatment of psoriasis includes few immunosuppresive drugs which can lead to exacerbation of symptoms of covid or increase the risk of disease severity.
So, yes psoriasis can be called as a '' risk factor ".
2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?
A) Immunosuppressive drugs can cause various long tern effects if used for a long time, some of these complications are:
Elevated pressure in the eyes (glaucoma)
Clouding of the lens in one or both eyes (cataracts)
A round face (moon face)
High blood sugar, which can trigger (New onset diabetes) or worsen diabetes
Increased risk of infections, especially with common bacterial, viral and fungal(mucormycosis) microorganisms.
Thinning bones (osteoporosis) and fractures
Suppressed adrenal gland hormone production that may result in a variety of signs and symptoms, including severe fatigue, loss of appetite, nausea and muscle weakness
Thin skin, bruising and slower wound healing
3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?
A) NO, disease per say causes the fibroproliferative response. Mechanical ventilation just supports the lungs.
CASE9)
Covid with de novo Diabetes
Link to Case report log:
https://vidya36.blogspot.com/2021/05/a-45-year-old-female-with-viral.html
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 )?
A) A possible hypothesis is that the “Severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2)” may affect the pancreatic β-cells producing a reduction of insulin secretion. At the same time, the infection is also accompanied by a huge production of cytokines, which may induce insulin resistance. Both, reduced insulin secretion and insulin resistance, may hesitate in hyperglycemia. This is therefore Type-2 diabetes.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7445137/#:~:text=A%20possible%20hypothesis%20is%20that,which%20may%20induce%20insulin%20resistance.
2.Could it be steroid induced Diabetes in this patient?
A) Yes, it is possible for patients to develop steroid induced diabetes, even when treated for a short time, which can result in type 2 DM, which may or maynot subside.
PATHOPHYSIOLOGY:
Increase in insulin resistance with increased glucose production and inhibition of the production and secretion of insulin by pancreatic β-cells
Corticosteroids increase endogenous glucose production, increment in gluconeogenesis and antagonizing the metabolic actions of insulin
Enhance the effects of other counterregulatory hormones, such as glucagon and epinephrine, which increase the endogenous synthesis of glucose
Also been shown that the expression of the nuclear receptor peroxisome proliferator-activated receptor α is necessary for the increment in endogenous glucose production induced by corticosteroids
Corticosteroids reduce peripheral glucose uptake at the level of the muscle and adipose tissue
Costicosteroids also inhibit the production and secretion of insulin from pancreatic β-cells and induce β-cell failure indirectly by lipotoxicity
CASE10)
Comparing two covid patients with variable recovery
Case report log: https://vidya36.blogspot.com/2021/05/comparative-study.html?m=1
1.What are the known factors driving early recovery in covid?
A) Factors responsible for early recovery are:
Innate immunity
adaptive immunity
past exposure to any of these endemic viruses (HCoV-229E, HCoV NL-63, HCoV-OC4, HCoV-HKU1) which show sequence homology of structural proteins in SAR-Co V and MERS-CoV. Thus, the possibility of a protective cross-immunity in the Indian population against COVID-19 cannot be ignored in explaining a rather mild effect of the current coronavirus pandemic in India in comparison to that in Europe and the USA.
Malaria endemicity might have a role to play. It is plausible that persons in malaria-endemic zones, which may also be endemic for several tropical pathogens including viruses, have recurrent cytokine fluctuations in response to minor and subclinical infections. These recurrent fluctuations may have a de-sensitizing effect on the body’s immune system, which prevents an uncontrolled and detrimental immune response and thus severe clinical disease in SARS-CoV-2 infection.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220291/
CASE11)
Covid moderate with first time detected diabetes:
Link to Case report log :
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?
A) Diabetes can definitely worsen the prognosis of a COVID patient, as increased sugar levels can help the viruses to thrive for a longer time in the body.
Factors which can precipitate diabetes in covid patients can be:
Cytokine storm destroying the pancreatic beta cells, leading to lower levels of insulin.
Virus entering through ACE-2 receptors in the lung tissue, and destroying these receptors which are also present in pancreatic tissue, thereby causing decreased levels of insulin, thereby causing hyperglycemia.
lets not forget the STEROIDS, which induce hyperglycemia by various mechanisms, not only worsening the condition of already diabetic patient, but also causing NEW ONSET DIABETES.
2) Why couldn't the treating team start her on oral hypoglycemics earlier?
A) As the patient didn't have any hyperglycemia before, only when her sugars became uncontrolable she was started on fast acting insulin, ACTRAPID.
Case 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 bioclinical markers in this patient
that may have predicted the prolonged course of her illness?
· CRP
Rise in CRP indicate a more severe outcome later and more reliable for early
identification of case severity
· NLR(Neutrophil-to-lymphocyte-ratio)
High NLR suggest more severe outcome
· Lactate dehydrogenase
High levels of LDH suggest more necrosis of lung tissue and pneumonia and
severe disease that causes prolonged stay
· D-dimer
D-dimer is measure of coagulation and fibrinolysis activity. With
increase in D-dimer there is increased risk of mortality and morbidity
Reference : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219356/#!po=20.1220
Case 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?
· Increased hospital stay
· Increased risk of mortality
· Increased risk of complications
2. Does
the significant rise in LDH suggests multiple organ failure?
Yes, Extremely
high levels of LDH isoenzymes can indicate multi organ failure
Reference https://www.healthline.com/health/lactate-dehydrogenase-test#test
3.What is the cause of death in this case?
· The patient has elevated SGPT, SGOT
and ALP which indicate there is liver damage
·
SGOT:170 IU/lit
·
SGPT:444 IU/lit
·
ALP:303 IU/lit
· Serum LDH was very high indicating tissue
damage
serum LDH:835 IU/lit
· CRP is positive
· D-dimer level is elevated D-dimer:560ng/ml
· Blood urea is very high indicating
failing kidneys
Blood urea:87mg/dl
So the
possible cause of death is due to liver and kidney failure along with coagulation
and fibrinolysis or multiple organ failure
Case 14)
Long covid with sleep deprivation and ICU
psychosis
Link to Case report log:
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?
ICU psychosis can be assessed by Confusion
Assessment Method (CAM)-ICU-7 delirium severity scale.
Reference:
2)What are the risk factors in the patient that has driven
this case more towards ICU pyschosis?
· Prolonged stay at hospital and he has changed 3 different
hospitals which might have caused anxiety in him
· He was isolated environmentally which may be a reason
3)The patient is sleep deprived during his hospital stay..Which
do u think might be the most propable condition?
A) Sleep deprivation causing ICU pyschosis
B) ICU psychosis causing sleep deprivation
· During ICU stay, the lights, machines beeping, waking up to
take the medicines may impact the sleep of the patient and this might also be a
cause for ICU psychosis and
· The patient due to ICU psychosis may be in a state of
delirium talking to himself not oriented to time which might be the most
probable condition
4) What are the drivers toward current
persistent hypoxia and long covid in this patient?
· Pneumonia secondary to Covid 19 may drive towards persistent
hypoxia after being Covid negative
· Groundglass appearance of nearly 75% of both lungs
· Elevated LDH, CRP,D-dimer all are risk factors for prolonged
Covid infection
References : https://link.springer.com/article/10.1007/s12028-019-00795-4
Case 15)
Moderate Covid with comorbidity (Trunkal obesity and recent
hyperglycemia)
Link to Case report Log:
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 transient rise in blood glucose?
Yes, due to
the use of steroids in non diabetic Covid patient can increase blood sugars
transienlty until the usage has stopped
2. If
yes, can this transient rise lead to long term complication of New-onset
diabetes mellitus?
Hyperglycemia
in non-diabetic Covid patient can be a risk factor for diabetes but it is still
unclear about it
Reference : https://covidiab.e-dendrite.com/introduction.html
3. can this adversely affect the prognosis of the
patient?
· Diabetes is one of the most relevant co-morbidity
in worsening the prognosis of COVID-19 [1]. Data is also showing that hyperglycemia, in both people
with or without diabetes, is an important risk factor for death in COVID-19
· hyperglycemia in people with diabetes at the time
of hospital admission is more relevant as risk factor than the previous
glycemic control evaluated by HbA1c
· hyperglycemia at the admission in hospital seems
worsening the prognosis of COVID-19 more in people without diabetes than in people
with diabetes
Reference : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7445137/#:~:text=Diabetes%20is%20one%20of%20the,COVID%2D19%2C%2C%2C.
3.How can this transient hyperglycemia be treated to avoid complications and bad prognosis?
1.
| https://www.nature.com/articles/s41574-020-00435-4/figures/4 |
Reference : https://www.nature.com/articles/s41574-020-00435-4#Tab2
2. 4.What
is thrombophlebitis fever?
Phlebitis, if mild, may or may not
cause symptoms. Pain,
tenderness, redness (erythema), and bulging of the vein are common symptoms of
phlebitis. The redness and tenderness may follow the course of the vein under
the skin.
Low grade fever may
accompany superficial and deep phlebitis. High fever or drainage
of pus from the site of thrombophlebitis may suggest an
infection of the thrombophlebitis (referred to as septic thrombophlebiti
3. 5..Should the infusion be stopped inorder to control the infusion thrombophlebitis? What are the alternatives?
· The
development of superficial thrombophlebitis frequently complicates the
insertion of needles into
the veins for catheters to give medication or fluids in hospitalised patients.
The best treatment for these blood clots in the hands and arms remains unclear.
While local treatment has the potential to improve the painful symptoms and
patient discomfort, it may not prevent complications, including infection or
the extension or transit of the clot into the deep vein system.
· The
evidence about the treatment of acute infusion superficial thrombophlebitis is
limited and of low quality. Data appear too preliminary to assess the
effectiveness and safety of
topical
treatments, systemic anticoagulation or oral non‐steroidal
anti‐inflammatory drugs.
Case 16)
Mild to moderate covid with hyperglycemia
https://vaishnavimaguluri138.blogspot.com/2021/05/viral-pneumonia-secondary-to-covid-19.html
QUESTIONS:
1. 1.What could be the possible factors implicated in elevated
glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?
· The possible mechanisms of COVID-19 causing
abnormal glucose metabolism include islet β cell damage and insulin resistance.
Previous studies have reported that some viruses can directly cause pancreatic
β-cell damage [11], [12], and angiotensin converting enzyme 2 (ACE2) as a SARS-CoV-2
receptor has higher expression in pancreatic endocrine tissues than in exocrine
tissues
Reference https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7233217/#!po=39.1892
2. 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?
 |
It is still unclear about the type of diabetes following Covid infection
3. 3.How
is the prognosis in such patients?
Elevated HbA1c usually leads to severe disease
4. 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 of glucose
metabolism that acutely occur with severe COVID-19 will persist after
resolution of COVID-19, or remit when the infection resolves.
https://covidiab.e-dendrite.com/introduction.html
5)
Why didn't we start him on Oral hypoglycemic agents earlier?
Might be
because he was non diabetic and they did not suspect diabetes in him
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,covid infection in hypertensives can lead to severe infection.
• ACE2 is a modulator of the RAAS. The end product of the RAAS, angiotensin II, is a key vasoactive hormone that binds to angiotensin II receptor type 1 (AT1) located in the heart, lungs, blood vessels, kidneys, and adrenal glands, and it plays a central role in myocardial hypertrophy and fibrosis, inflammation, vascular remodeling, and atherosclerosis , by this binding it increases blood pressure. ACE2 is expressed in many human tissues including the nasal epithelium, heart, kidneys, and lungs, and inactivates angiotensin II diminishing its vasoconstrictive and myoproliferative effects.
SARS-CoV-2 binds to the ACE2 receptor via its spike protein to allow entry into host cells. This complex is endocytosed leading to down-regulation of ACE2 and resulting in local accumulation of angiotensin II. Severe respiratory illness is a hallmark of COVID-19 and a primary cause of morbidity- and mortality-local activation of the RAAS is proposed as a mechanism for severe lung injury.
2)what is the cause for pleural effusion to occur??
infection causes local inflammatory reaction resulting in increased capillary microvascular permeability and a rapid outpouring of fluid containing inflammatory cells into the pleural space
COVID CASE 18
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?
• It may be due to pulmonary capillary leakage in lungs , in response to epithelial endothelial damage due to covid infection.
•
https://pubmed.ncbi.nlm.nih.gov/33411411/2. What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?
3. What is the reason for Cardiomegaly?
• Direct Myocardial Cell Injury
The interaction of SARS-CoV-2 with ACE2 can cause changes to the ACE2 pathways, leading to acute injury of the lung, heart, and endothelial cells. A small number of case reports have indicated that SARS-CoV2 might directly infect the myocardium, causing viral myocarditis. However, in most cases, myocardial damage appeared to be caused by increased cardiometabolic demand associated with the systemic infection and ongoing hypoxia caused by severe pneumonia or ARDS
https://www.ncbi.nlm.nih.gov/books/NBK556152/
4. What other differential diagnoses could be drawn if the patient tested negative for covid infection?
• Influenza
• Mycoplasma pneumonia
• Parainfluenza
• Respiratory syncytial virus
• Streptococcus pneumonia
• Other viral or bacterial pneumonia.
5. Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?
• It is well known that D-dimer are produced during fibrin breakdown and serve as a marker of fibrinolytic activity. A relationship between proinflammatory cytokines and markers of activation of the coagulation cascade, including D-dimer, has been demonstrated in critical patients or patients with sepsis .There is also evidence that under inflammatory conditions, the alveolar haemostatic balance is shifted towards a predominance of prothrombotic activity .In addition, pro-inflammatory cytokines may be involved in endothelial injury, and may activate coagulation and inhibit fibrinolysis in patients with severe sepsis.
• D-dimer can be elevated such as in pregnancy, inflammation, malignancy, trauma, liver disease (decreased clearance), heart disease, sepsis or as a result of hemodialysis, CPR or recent surgery)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7286212/#:~:text=It%20has%20been%20reported%20that,patients%20with%20good%20clinical%20prognosis
COVID CASE 19
19)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???
There is still no proper studies undertaken , I couldn’t find any results that have been yet published on steroid adverse effect increases death rate among covid patients
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7391982/
2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically???
• In covid patients, immune system is reacting very strongly to the pneumonia, and the lungs are full of immune cells that produce cytokines. In turn, these cytokines act on liver to make clotting proteins. The inflammatory mechanism leads to what we call a “prothrombotic state.”
• The main clotting protein in the blood is fibrinogen. It’s soluble, and we have 2–4 grams per liter in your blood.
• The clotting factors switch soluble fibrinogen to insoluble fibrin, and that is the clot.
• The level is 2–4 grams per liter in most people. If you are pregnant, or as you get older, the levels get higher. They might go up to 5, 6, or even 7 [grams per liter].
But in COVID-19 We are seeing levels of 10, even 14 grams per liter.
And in covid 19 there is clotting occuring even in the tiny blood vessels which is not getting disolved with the normal dose anticoagulants which may increase chances of dying.(MAY BE INCREASING DOSE CAN PREVENT DEATH).
https://www.medicalnewstoday.com/articles/blood-thinners-may-protect-against-covid-19-complications#Several-study-limitations
3)Does chronic alcoholism have effect on the out come of Covid infection????
If yes,how??
Yes,chronic intake of alcohol alters the body's immune mechanism.
Chronic ethanol abuse almost doubles the risk of developing acute respiratory distress syndrome . Following are the mechanisms:
- reducing the number of T lymphocytes - by preventing proliferation and by altering cell turnover;
- favoring a pro-inflammatory status through an increased level of proinflammatory cytokines, such as tumor necrosis factor alfa (TNF α) and interleukins 1 and 6 (IL-1, IL-6);
- decreases the function and number of NK (Natural Killers) cells responsible for removing infected or malignant cells;
- disturbance of macrophage functions in the lung alveoli;
- damage to the respiratory ciliated cells which plays an essential role in filtering pathogenic microorganisms.
Another important factor is malnutrition secondary to excessive alcohol intake .The harmful effect on the mucosa of the digestive tract consists in decreasing the absorption and metabolism of certain nutrients, including B vitamins (B1, B6 and B9 or folic acid), leading to a slowing of leukocyte proliferation and differentiation . The defense mechanisms of the mucosal immune system are also affected, resulting in a dysfunction of the function of IgA and IgG immunoglobulins, which are responsible for local protection against infectious agents
COVID CASE 20
20) 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?
• In human monocytes, elevated glucose levels directly 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 might support viral proliferation. In accord with this assumption, hyperglycaemia or a history of T1DM and T2DM were found to be independent predictors of morbidity and mortality in patients with SARS-COV-2.
• Also there is altered immune system in diabetics.
https://www.nature.com/articles/s41574-020-00435-4
2. In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?
• Two experimental agents (dexamethasone and hydroxychloroquine) have shown some promise as treatment agents.
• Combined treatment with these two agents might be more beneficial than either agent alone. However, it should be kept in mind that the efficacy of dexamethasone in treating COVID-19 was proven in well-designed RCTs such as the RECOVERY study , whereas no such compelling RCTs have been performed for hydroxychloroquine.
3. What effect does a history of CVA have on COVID prognosis?
• In all the case series studied, history of stroke was associated with poorer progression of COVID-19. In a cohort of patients from 55 hospitals, history of stroke was twice as frequent among patients classified as having severe COVID-19 than among patients with mild symptoms. The virus enters the brain parenchyma, endothelium, and heart, and alters coagulation, which may lead to stroke
• The virus enters the brain parenchyma, endothelium, and heart, and alters coagulation, which may lead to stroke.
• History of stroke is associated with a three-fold increase in the risk of death due to SARS-CoV-2 infection
COVID CASE 21
21) 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?
• Comorbidities like
• Diabetes mellitus since 7years
• Asthma since 7 years
• History of pulmonary kochs which might have caused some lung damage.
• History of pneumonia might have caused damage in lungs.
• Chronic kidney disease since 2yrs.
2)Can you explain why the D dimer levels are increasing in this patient?
• D dimer is a product after clot is degraded.
• In covid 19 infection,thrombotic events takes place due to release of clotting factors
In response to cytokines release.
• May be in this patient also,cytokine release led to prothrombotic events and fibrinolytic events which led to increased d dimer levels.
3)What were the treatment options taken up with falling oxygen saturation?
• 15 litres of oxygen/minute was given
• Patient was intubated when oxygen saturation fell to 30%.
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)
• Diabetes might have caused the CKD , Diabetes induces structural changes, including thickening of the glomerular basement membrane, fusion of foot processes, loss of podocytes with denuding of the glomerular basement membrane, and mesangial matrix expansion.
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