1) Covid 19 with co morbidity (Pulmonology/Rheumatology)
https://nikhilasampathkumar.
Q1)How does the pre-existing ILD determine the prognosis of this patient?
In patients with preexisting ILD, COVID-19 infection has led to acute exacerbation of underlying ILD.
The criteria for ILD exacerbation include:
1) subacute worsening of dyspnea
2) hypoxemia
3)new pulmonary infiltrates on imaging
4)absence of pulmonary emboli
5)cardiac failure
6) other non-pulmonary causes
Thus it leads to a poor prognosis
Q2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism?
Corticosteroids manages the disease flares and for initial treatment of RA
glucocorticoids are significant risk factor for bacterial infections.
Glucocorticoid use doubled the rate of serious bacterial infections in a dose-dependent manner as compared with methotrexate
It is concluded that there is no evidence to support its use in COVID-19, and it may in fact lead to more harm than good
Q3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?
In Covid
lymphoplasmocyte cell infiltrates are involved (mainly at the lung level),
the expression of pro-inflammatory cytokines such as interleukin (IL) IL-1, IL-6, IL-17, and TNF-α, and markers of systemic inflammation such as C-reactive protein or ferritin
A parallelism of events was found with RA, where there are similar infiltrates at the synovial level, with expression of the same group of proinflammatory cytokines and elevation of acute-phase reactants
. However, this route is unlikely, given that there has been no increase in exacerbations of RA patients concomitantly suffering from COVID-19
Q4) Why was she prescribed clexane (enoxaparin)?
Clexane 60mg Injection is an anticoagulant
It is used to prevent and treat harmful blood clots.
It stops the existing clots from getting any bigger and restricts the formation of any new clot.
It is also helpful in the prevention of blood clots in veins, a condition called deep vein thrombosis, and pulmonary embolism.
2) Covid 19 with Diabetes
Q1) 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?
Novel coronavirus enters cell hosts through An- giotensin II Converting Enzyme receptor (ACE2).
ACE2 receptor is found in the pancreas, both on exocri- ne cells and in the endocrine cells, that constitute pan- creatic islets.
Interestingly, its expression is also rele- vant in the endothelial cells of the microvasculature supplying beta-cells that produce insulin.
deficiency of this receptor compromises the vasculature in pancreatic islets, thus decreasing its endocrine function.
cytokine storm - caused by the severe inflammatory response taking place in the lungs - also targets the pancreas possibly causing diabe- tes
Q2) Did the patient's diabetic condition influence the progression of her pneumonia?
COVID-19 and diabetes, but no other comorbidities (n = 24)
were at higher risk for severe pneumonia, release of tissue injury-related enzymes, excessive uncontrolled inflammation responses and hypercoagulable state associated with dysregulation of glucose metabolism when compared with patients without diabetes.
Q3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?
predict which COVID-19 patients have poorer outcomes.
The D-dimer molecule is a product of the degradation of the fibrin protein.
A biomarker-based evaluation which identifies the amount of ongoing coagulation at a given point of time
.D-dimer has been shown to be an indicator for cardiac injury in COVID-19 patients in a setting of prothrombotic state
D-dimer may be able to predict which COVID-19 patients have poorer outcomes.
3) Covid 19 Severe
Q1). Why was this patient given noradrenaline?
Noradrenaline, is a medication used to treat people with very low blood pressure. Noradrenaline is a vasoconstrictor that predominantly stimulates α1 receptors to cause peripheral vasoconstriction and increase blood pressure.
It also has some β1 receptor agonist activity that results in a positive inotropic effect on the heart at higher doses.1,2
Q2) What is the reason behind testing for LDH levels in this patient?
LDH is an intracellular enzyme found in cells in almost all organ systems, which catalyzes the interconversion of pyruvate and lactate, with concomitant interconversion of NADH and NAD+
Lactate dehydrogenase (LDH) is one such biomarker of interest, especially since elevated LDH levels have been associated with worse outcomes in patients with other viral infections in the past
there was a >6-fold increase in odds of severe disease and a >16-fold increase in odds of mortality in patients with elevated LDH.
Q3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
BiPap may not be a good option if your breathing is very poor. It may also not be right for you if you have reduced consciousness or problems swallowing
Therefore patient might have got shifted to Mechanical ventilation
Advantages of Mechanical ventilation
The patient does not have to work as hard to breathe – their respiratory muscles rest.
The patient's as allowed time to recover in hopes that breathing becomes normal again.
Helps the patient get adequate oxygen and clears carbon dioxide.
Preserves a stable airway and preventing injury from aspiration.
4) Covid 19 Mild
https://gsuhithagnaneswar.
Q1). Is the elevated esr due to covid related inflammation?
Erythrocyte sedimentation rate (ESR) is a blood test. It measures how quickly erythrocytes, or red blood cells, separate from a blood sample that has been treated so the blood will not clot.
The sustained high level of ESR possibly brings a negative effect on COVID-19 patients' prognosis
However the elevation in esr cannot be explained based on the present knowledge on Covid
Q2) What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization?
After 14 days of isolation he got tested again for COVID-19 which was positive
He then developed fever since 4 days,
cough which was productive since 4 days
shortness of breath grade 3 since 2 days.
He also had fatigue.He lost the sense of taste and smell.
Since the patient has SOB of grade 3. This poses a challenge for home isolation.
Patients with COVID-19 had almost 19 times the risk for acute respiratory distress syndrome (ARDS) than did patients with influenza, (adjusted risk ratio [aRR] = 18.60; 95% confidence interval [CI] = 12.40–28.00), and more than twice the risk for myocarditis (2.56; 1.17–5.59), deep vein thrombosis (2.81; 2.04–3.87), pulmonary embolism (2.10; 1.53–2.89), intracranial hemorrhage (2.85; 1.35–6.03), acute hepatitis/liver failure (3.13; 1.92–5.10), bacteremia (2.46; 1.91–3.18), and pressure ulcers (2.65; 2.14–3.27). The risks for exacerbations of asthma (0.27; 0.16–0.44) and chronic obstructive pulmonary disease (COPD) (0.37; 0.32–0.42) were lower among patients with COVID-19 than among those with influenza. The percentage of COVID-19 patients who died while hospitalized (21.0%) was more than five times that of influenza patients (3.8%), and the duration of hospitalization was almost three times longer for COVID-19 patients.
5) Covid 19 and comorbidity (Altered sensorium, azotemia, hypokalemia)
Q1) What was the reason for coma in this patient?
The patient has an spo2 of 20%. This might have lead to cerebral hypoxia thus leading to coma.
Also, low blood potassium can make you short of breath, as it can cause the heart to beat abnormally. This means less blood is pumped from your heart to the rest of your body
Thus low spo2 and thus coma
Q2) 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?
Hospital 1 might not have correlated Severe weakness of 4 limbs with low values of potassium which hospital 2 has diagnosed.
Yes, coma is related to Hypokalemia periodic paralysis as it might have caused cerebral hypoxia
3) How may covid 19 cause coma?
After cessation of sedatives, the described cases all showed a prolonged comatose state.
unconsciousness after prolonged periods of mechanical ventilation in the ICU.
6) Severe Covid 19 with altered sensorium
1. What was the cause of his altered sensorium?
any of the following reasons
An altered state is any mental state(s),
induced by various physiological( increased hospital stay) ,
psychological( mental depression due to isolation),
pharmacological maneuvers or agents( drugs of COVID)
2. What was the cause of death in this patient?
This patient is an elderly chronic alcoholic and smoker.
This might have delayed his healing process thus causing death
Also he had elevation LFT and RFT values
7) Covid 19 Moderate with ICU psychosis
https://drsaranyaroshni.
Q1)What is the grade of pneumonia in her?
Q2)What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?
Q3)What all could be the factors that led to psychosis in her ?
Q4)In what ways shall the two drugs prescribed to her for psychosis help ?
Q5)What all are the other means to manage such a case of psychosis?
Q6)What all should the patient and their attendants be careful about ( w.r.t. COVID )after the patient is discharged ?
Q7)What are the chances that this patient may go into long covid given that her "D Dimer" didn't come down during discharge?
8) Covid 19 Moderate
Q1. Can psoriasis be a risk factor for severe form of COVID?
Elderly psoriasis patients and/or patients using conventional immunosuppressive regimens and biologic agents are at higher risk for infectious diseases.
But the frequency of COVID-19 does not increase in patients using immunosuppressants, including those receiving biological therapy with a diagnosis of psoriasis
2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?
According to the present knowledge on Covid,there is no indication that people taking immunomodulatory drugs for other diagnosed conditions should be concerned that their medication increases their risk for severe COVID-19,"
3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?
patients of Covid with greater fibrotic changes required more prolonged mechanical ventilation, and this in turn was associated with an increased severity of systemic organ failure.
Hence Mechanical ventilation is risk factor
9) Covid with de novo Diabetes
https://vidya36.blogspot.com/
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)?
It is most probably the type -1 diabetes ,developed due to viral infection and cytokine storm induced damage to pancreas might have caused the diabetes .!so it could be virus induced type -1 DM
Q2)Could it be steroid induced Diabetes in this patient?
There is a chance for steroid induced diabetes too but it doesn’t seem much significant when compared to virus induced diabetes
10) Comparing two covid patients with variable recovery
Q1)What are the known factors driving early recovery in covid?
These might be the factors responsible for early recovery of Covid:
1. Better immune response of the patient
2. Good food habits prior to And during the Covid period
3. Early detection of symptoms and thus using medication
4. Age related (Elderly have a slow recovery than young)
5. Maintaining hygiene even after Covid infection
6. Mental strength
7. Health related (patient with Comorbidities have slow recovery)
11) Covid moderate with first time detected diabetes:
https://rishithareddy30.
Q1) 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?
Hypertension and severe obesity are common comorbidities in patients with diabetes. It is unclear whether diabetes alone contributes to increased risk of morbidity and mortality related to COVID-19. have indicated that poorer glycemic control is associated with poorer outcomes in people with diabetes
mechanisms that may increase the ability of COVID-19 to impact patients with diabetes:
higher affinity cellular binding and efficient virus entry; decreased viral clearance; diminished T-cell function; increased susceptibility to hyperinflammation and cytokine storm; and the presence of cardiovascular disease
pathogenetic link between diabetes and COVID-19. Both disease conditions involve inflammation with the release of inflammatory markers. The roles of angiotensin-converting enzyme molecule and dipeptidyl peptidase were explored to show their involvement in COVID-19 and diabetes. Pathogenetic mechanisms such as impaired immunity, microangiopathy, and glycemic variability may explain the effect of diabetes on recovery of COVID-19 patients. The effect of glucocorticoids and catecholamines, invasion of the pancreatic islet cells, drugs used in the treatment of COVID-19, and the lockdown policy may impact negatively on glycemic control of diabetic patients.
Patients with diabetes mellitus have increased predisposition to viral and bacterial infections including those affecting the respiratory tract
One of the mechanisms responsible for this predisposition is the “lazy” leukocyte syndrome, which represents impaired leukocyte function of phagocytosis (impaired immunity). This further emphasizes the likelihood of increased propensity of SARS-CoV-2 infections in diabetic cohorts
Microangiopathy in diabetes mellitus also impairs the lung compliance with consequent affectation of the gaseous exchange. This impairment may result in the proliferation of some respiratory pathogens including SARS-CoV-2
There are respiratory changes in diabetic patients that affect lung volumes and pulmonary diffusing capacity
Glycemic variability is a prognostic factor in diabetic patients with COVID-19 infection. Hyperglycemia worsens the outcome by the process of cytokine storm, endothelial dysfunction, and multiple organ injuries
In the lungs, the primary target of COVID-19, hyperglycemia leads to a rapid deterioration in spirometric functions, especially decreased forced expiratory volume in 1 second and forced vital capacity
hyperglycemic states, there is elevated glucose concentration in the respiratory epithelium which may affect its innate immune capacity. Hypoglycemia also increases cardiovascular mortality by accentuating monocytes which are pro-inflammatory and enhancing platelet aggregation
Severe hypoglycemia which may occur with strict glycemic control may worsen the overall mortality rate
suboptimal glycemic control in COVID-19 patients is correlated with higher mortality rate
Effect of COVID-19 on Diabetes:
COVID-19 infection compounds the stress of diabetes mellitus by releasing glucocorticoids and catecholamines into circulation. These worsen glycemic control and increase the formation of glycation end products in many organs and worsen prognosis
The degree of inflammatory response to COVID-19 is more marked in diabetic patients than in nondiabetic cohorts
showed that type 2 diabetic group had higher levels of inflammatory markers such as C-reactive protein and procalcitonin (57.0 and 33.3%) than the nondiabetic group (42.4 and 20.3%), respectively. Elevated C-reactive protein may serve as a marker for identifying those with high risk of death from COVID-19
D-dimer which is a marker of coagulation status was also elevated in the diabetic group compared to the nondiabetic group
The levels of these inflammatory markers have been correlated with the severity of COVID-19 infection
2) Why couldn't the treating team start her on oral hypoglycemics earlier?
To control the high range diabetes she is on insulin’s injections which have faster and effective action to control diabetes than oral hypoglycaemic drugs.
Insulin exhibits inhibitory action on ADAM-17 [35]. ADAM-17 enhances the proteolytic shedding of the enzymatic active ecto-domain of ACE2. This may suggest that insulin increases the activity of ACE2 [35] and also increases the infectivity of SARS-CoV-2
The beneficial effect of insulin may be related to its anti-inflammatory effect, which is by suppression of pro-inflammatory cytokines and increased immune mediators
Insulin use has effective glycemic control.which benefits a better prognostic results
.12) Moderate to severe covid with prolonged hospital stay:
Q1) What are the potential bioclinical markers in this patient that may have predicted the prolonged course of her illness?
The potential biochemical markers in this patient are
Elevated levels of
LFT- Total bilirubin : 1.24 mg/dl
Direct bilirubin : 0.67 mg/dl
SGOT : 73 units/ lit
SGPT : 80 units/ lit
ALP : 342 units/ lit
RFT Blood urea : 34 mg/dl
Sodium : 150 meq/lit
Potassium : 5.2 meq/lit
SERUM LDH 571 units/lit
FBS 332 mg /dl
13) Severe covid with first diabetes
https://vignatha45.blogspot.
Q1)What are the consequences of uncontrolled hyperglycemia in covid patients?
•Severe inflammatory changes in lungs in case of covid pneumonia.
•Delayed recovery of the patient .
Since elevated blood sugar levels favors the virus growth and multiplication.
Q2)Does the significant rise in LDH suggests multiple organ failure?
High LDH levels
Extremely high levels of LDH could indicate severe disease or multiple organ failure. Because LDH is in so many tissues throughout the body, LDH levels alone won't be enough to determine the location and cause of tissue damage.
Q3)What is the cause of death in this case?
Cause of death could be most probably due to:
•Severe covid pneumonia associated with uncontrolled hyperglycaemia
•Multiple organ failure
14) Long covid with sleep deprivation and ICU psychosis
1)Which subtype of ICU psychosis did the patient land into according to his symptoms?
The subtype of icu psychosis in this patient is of HYPERACTIVE
It is characterized by agitation, restlessness, emotional lability, and positive psychotic features such as hallucinations, illusions that often interfere with the delivery of care. It should be remembered that new-onset psychotic symptoms in older adult patients are unlikely to be a primary mental illness, and search for a pharmacological or physiological cause should be carried out.
2)What are the risk factors in the patient that has driven this case more towards ICU pyschosis?
There are more chances for a Covid patient to be landing into ICU psychosis if he has any of these Major complications being 1) cardiovascular diseases 2) hypertension and 3) cerebrovascular diseases
Since this patient is a known case of htn since 2 years and had a cerebrovascular episode 2 years back
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
The most probable condition in this case might be SLEEP DEPRIVATION CAUSING ICU PSYCHOSIS
these might be have caused sleep disturbance and thus lead to icu pyschosis:
Environmental contributors include patient care, noise, light, and medications.
Patient factors, including illness severity, SOB can also play important roles
4) What are the drivers toward current persistent hypoxia and long covid in this patient?
The pneumonia that COVID-19 causes tends to take hold in both lungs. Air sacs in the lungs fill with fluid, limiting their ability to take in oxygen and causing shortness of breath, cough and other symptoms.
While most people recover from pneumonia without any lasting lung damage, the pneumonia associated with COVID-19 can be severe. Even after the disease has passed, lung injury may result in breathing difficulties that might take months to improve.
This might be the cause for persistent hypoxia in this patient
15) Moderate Covid with comorbidity (Trunkal obesity and recent hyperglycemia)
Q1. As the patient is a non- diabetic, can the use of steroids cause transient rise in blood glucose?
Yes, Increase in the blood glucose might be due to the use of steroids, in this case Dexamethasone
2. If yes, can this transient rise lead to long term complication of New-onset diabetes mellitus?
High blood glucose levels whilst taking steroids may subside after one stop taking steroids, however, some people may develop type 2 diabetes which will need to be managed for life.
Type 2 diabetes is more likely to develop following longer term usage of steroids, such as usage of oral corticosteroids for longer than 3 months.
3. How can this adversely affect the prognosis of the patient?
The reason for worse prognosis in people with diabetes is likely to be multifactorial, thus reflecting the syndromic nature of diabetes. Age, sex, ethnicity, comorbidities such as hypertension and cardiovascular disease, obesity, and a pro-inflammatory and pro-coagulative state all probably contribute to the risk of worse outcomes
4. How can this transient hyperglycemia be treated to avoid complications and bad prognosis?
At admission: pre-meal BG: 150 to 180 mg/dl and/or post-meal BG 200 to 250 mg/dl)
If there is an anticipated delay in consulting endocrinologist/physician, initiate on Tab Metformin (either immediate or sustained release) 500 mg BD
Gliptin (Tab Vildagliptin 50 mg BD or Tab Sitagliptin 100 mg OD or Tab Linagliptin 5 mg OD or Tab Teneligliptin 20 mg OD)
Indication: At admission: pre-meal BG: ≥180 mg/dl or post-meal BG ≥250 mg/dl
A. Total daily dose (TDD) = 0.4 units/kg/day (age > 65 yr, nephropathy or liver disease, use 0.2 units/kg/day)
B. Total daily dose is divided equally into 4 doses (25% each): 3 doses are for bolus insulin (Regular insulin 30 min before breakfast, before lunch and before dinner) and 1 dose for basal insulin (Inj. NPH insulin at bed time/ 2 hours after dinner)
If pre-meal BG value is 140 to 180 mg/dl and/or post-meal BG value is 180 to 250 mg/dl → consult endocrinologist/physician for OAD optimization
B. If pre-meal BG value ≥180 mg/dl and/or post-meal BG value ≥250 mg/dl despite being on OAD → start basal-bolus insulin regimen using calculation mentioned in section 3A (Kindly note that in this particular scenario, OADs apart from Metformin and Gliptins need to be stopped).
5. What is thrombophlebitis fever?
Thrombophlebitis is when a blood clot Any veins and slows the blood flow in the vein. It may be due prolonged use of IV cannula.
This causes fever
6. Should the infusion be stopped inorder to control the infusion thrombophlebitis? What are the alternatives?
There is no need to stop infusion to control Theombophlebitis. Instead change the IV cannula to opposite or another site. If there is pain at that site use aspirin or ibuprofen
16) Mild to moderate covid with hyperglycemia
1. What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?
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?
3. How is the prognosis in such patients?
4. Do the alterations in glucose metabolism that occur with a sudden onset in severe Covid-19 persist or remit when the infection resolves?
5) Why didn't we start him on Oral hypoglycemic agents earlier?
17) Covid 19 with hypertension comorbidity
1)Does hypertension have any effect to do with the severity of the covid infection.If it is, Then how?
2)what is the cause for pleural effusion to occur??
18) Covid 19 with mild hypoalbuminemia
What is the reason for hypoalbuminemia in the patient?
Answer:
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.
Question 2:
What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?
Answer:
Yes, what the patient is experiencing is known as viral exanthem which is one of the cutaneous manifestation of COVID-19.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7549735/
Question 3:
What is the reason for Cardiomegaly?
Answer:
A possible cause can be Direct Myocardial Cell [1:36 AM, 5/31/2021] Abbas: ry. 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/
Question 4:
What other differential diagnoses could be drawn if the patient tested negative for covid infection?
Answer:
Possible alternative diagnoses may include:
• Influenza
• Mycoplasma pneumonia
• Parainfluenza
• Respiratory syncytial virus
• Streptococcus pneumonia
• Other viral or bacterial pneumonia.
Question 5:
Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?
Answer:
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.
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