I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis.
Following are my answers to the given assignment after comprehending the given clinical data.
1) Pulmonology
A) 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?
ANS: Considering recent scenario patient first developed grade 4 SOB due to lung pathology (COPD and brochiectasis) then as the disease progressed right heart failure occurred which lead to increased back pressure and decreased venous return which lead to ankle edema and facial puffiness. Patient might also have developed renal failure as the rtf was a bit abnormal and which might have also lead to facial puffiness and hypochloremia and hyponatremia. Due to decreased venous return there is decreased cardiac output leading to left heart failure which might have also aggravated her SOB. As more fluid is trapped in extra vascular space there may be decreased urine output due to ADH release. Primary etiology could be in her lungs.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS: O2 to maintain SP02, BIPAP to deliver O2 and to deliver O2 while expiration ,mamoxiclav and azithromycin antibiotic to resolve infection, lasix as diuretics for hypertension. Pantop is a PPI , hydrocortisone for bronchiectasis ,ipratropium bromide for air flow and dilation of air passage, pulmoclear to relieve the mucus, chest physiotherapy as exercise for lungs and to wash out accumulated CO2, insulin as patient is diabetic
3) What could be the causes for her current acute exacerbation?
ANS: Heart failure along with kidney failure
4. Could the ATT have affected her symptoms? If so how?
ANS: Could have effected as isoniazid is hepatotoxic
5.What could be the causes for her electrolyte imbalance?
ANS: Renal failure or heart failure could have caused her electrolyte imbalance
2) Neurology
A) Link to patient details:
1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS: talking as well as laughing to himself and unable to lift himself off the bed and move around, and had to be assisted he has history of GTCS seizures and alcohol withdrawal syndrome. Cause could be multifactorial 1.thiamine deficiency and due to 2.alcohol withdrawal as patient has high urea could be uraemia syndrome
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS: Thiamine for deficiency ,lorazepam for seizures, pregabaline for seizures, insulin for diabetes, lactulose for cheating ammonia, him as he has potassium deficiency ,ns as fluids
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
ANS: Could be because patient developed wet beri beri which hasn’t developed then
4) What is the reason for giving thiamine in this patient?
ANS: B1 deficiency is more common in chronic alcoholics and patient his left ventricle vas hypertrophic showing symptoms of wet beri beri.
5) What is the probable reason for kidney injury in this patient?
ANS : Can be because of alcohol
6). What is the probable cause for the normocytic anemia?
ANS: Could be due to nutritional deficiency or due to anemia of chronic disease.
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
ANS: Alcohol causes nutritional deficiency which delays the healing process and patient also has diabetes mellitus which delays healing process
B) 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?
ANS: giddiness This was associated with vomiting on the same day.
After 3 days he consumed a small amount of alcohol .developed giddiness getting up from the bed and while walking. This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus. He has associated vomiting
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS: MVT methyl cobalamine for B12 deficiency, aspirin as anti platelet, ondansetron for nausea and vomiting, clopidogrel as anti platelet, thiamine for B1 deficiency
3) Did the patients history of denovo HTN contribute to his current condition?
Ans) Might have contributed as the patient didn’t use medication and is a risk factor for stroke
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Ans) Yes it makes him susceptible for both hemorrhagic and ischemic stroke as he seems to be a chronic alcoholic and consumes more alcohol
C) 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?
ANS) The patient is a chronic hypokalemic. She was diagnosed with hypokalemia 10 years go when she developed both right and left limbs paralysis .One year back she was also diagnosed with cervical spondylitis when she went to a hospital with neck pain. Now she developed bilateral pitting edema and came to the hospital. It seems that her condition has been progressive. It might due to lack of proper diet or medication.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
ANS) Risk factors for hypokalemia in her- Female gender, usage of steroids,
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANS) ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression in more severe hypokalemia. Severe hypokalemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.
D) Link to patient details:
QUESTIONS:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
ANS: yes there is a relation between stroke and siezures. as in this patient stroke by causing ischemia and infraction may cause loss of brain parenchyma which is followed by a gliosis as a result of insult as a late response. Epileptic foci resulting from brain injury are characterized by areas of intense fibrillary gliosis bordering neuronal tissue. The known pathological changes that occur in gliosis may impair glial control of extracellular potassium ions and lead to excessively excitable neuronal border regions. It also decreases the seizure threshold. Seizures also increase the chances of having a recurrent infract which may lead to more brain tissue involvement. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury (particularly after carotid end arterectomy) is in acute onset seizures pathology
2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
ANS: Initially patient had a Focal seizures without loss of consciousness(simple partial seizures) which usually follow after trauma or stroke and in this patient due to temporal lobe involvement and gliosis it might have progressed to complex partial seizures or GTCS with more brain parenchyma involvement
E) Link to patient details:
Questions:
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
ANS: Alcohol related ataxia, the symptoms affect gait (walking) and lower limbs more than arms and speech. It can also cause associated signs of peripheral neuropathy. It may be due to injury to cerebellum or cerebrum due to intoxication and could also be due to thiamine deficiency. And frequent falls which are not attended by patients must have added to the effect
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
ANS: Chronic heavy and binge ethanol consumption is likely linked to the occurrence and clinical worse outcome of ICH and frequent falls might have aggravated.
F) Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
ANS) No, It might not be related to the past accident as it took place years ago.
2.What are warning signs of CVA?
- Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.
- Sudden confusion, trouble speaking, or difficulty understanding speech.
- Sudden trouble seeing in one or both eyes.
- Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
- Sudden severe headache with no known cause.
3.What is the drug rationale in CVA?
ANS) 1.Injection Mannitol 100ml/IV/TD
Mannitol is an osmotic diuretic, typically used at 0.25–0.5 g/kg IV administered over 15 minutes. It lowers intracranial pressure
2.TAB Ecospirin 75 mg po/OD
Aspirin irreversibly inhibits cyclooxygenase, which prevents the conversion of arachidonic acid to thromboxane A2 (TXA2). Thromboxane A2 is a vasoconstrictor and stimulator of platelet aggregration. Platelets are inhibited for their full life cycle (5–7 days) after exposure to aspirin. Aspirin also inhibits prostacyclin activity and this inhibits platelet aggregration. The effects of aspirin on prostacyclin are dose related.
3.TAB ATORVAS 40mg po/HS - To lower cholesterol levels.
4.BP/PR/TEMP/SP02 MONITORING (4th hourly)
Maintaining adequate tissue oxygenation is important during periods of acute cerebral ischemia in order to prevent hypoxia and potential worsening of the neurologic injury. Supplemental oxygen should be administered if there is evidence of hypoxia by blood gas determination or desaturation detected by pulse oximetry.
5.RT FEEDS-100ml milk with protein powder(2nd hourly)- Nutrition purpose
4. Does alcohol has any role in his attack?
ANS) ALcohol when taken is always a risk factor for stroke, but the patient does not seem to be a chronic alcoholic.
5.Does his lipid profile has any role for his attack??
ANS) The values seems to be near upper normal. So, the cause might not be his lipid profile. It could be one of the risk factor. This is could be a cryptogenic stroke.
G) Link to patient details:
Questions
1)What is myelopathy hand ?
ANS) There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi.This finding of weak finger adduction in cervical myelopathy also called the "finger escape sign".
3)What is Hoffman’s reflex?
ANS) The Hoffman sign is an involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down. The reflexive pathway causes the thumb to flex and adduct quickly. A positive Hoffman sign indicates an upper motor neuron lesion and corticospinal pathway dysfunction likely due to cervical cord compression. However, up to 3% of the population has been found to have a positive Hoffman without cord compression or upper motor neuron disease.
H) Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
ANS) Recurrent seizures(seizure clusters/status epilepticus)resolved secondary to cortical vein thrombosis with hemorrhagic venous infarction in right posterior temporal lobe with (4mm midline shift), microcytic hypochromic anemia being the risk factor.
2) What are the risk factors for cortical vein thrombosis?
- Sickle cell anemia.
- Chronic hemolytic anemia.
- Beta-thalassemia major.
- Heart disease — either congenital (you're born with it) or acquired (you develop it)
- Iron deficiency.
- Certain infections.
- Dehydration
- Clotting defects
3)There was seizure free period in between but again sudden episode of GTCS why? resolved spontaneously why?
ANS) Could be due to the clot that is intermittently stimulating cortex that were presenting as seizures
4) What drug was used in suspicion of cortical venous sinus thrombosis?
CLEXANE - Enoxaparin - LMWH is an anticoagulant which was used in suspicion of CVST.
3) Cardiology
A) Link to patient details:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
ANS) Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).
Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure. The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body.
2.Why haven't we done pericardiocenetis in this pateint?
ANS) Pericardiocentesis and pericardial biopsy are generally not useful in patients with small or moderate pericardial effusions, as a definitive diagnosis may not be provided. According to a study of 231 patients with acute pericarditis of unknown cause, pericardiocentesis provided the cause of pericarditis in 6% of cases and pericardial biopsy provided the diagnosis in 5% only. In contrast, in cases with pericardial tamponade, pericardiocentesis provided the diagnosis in 29% and pericardial biopsy provided a diagnosis in 54% of cases.6 Therefore, pericardiocentesis is often indicated in patients with pericardial tamponade and in patients with suspected purulent or neoplastic pericarditis.
3.What are the risk factors for development of heart failure in the patient?
- Smoking
- Alcohol
- Diabetes
- Hypertension
B) Link to patient details:
Questions:
1.What are the possible causes for heart failure in this patient?
ANS) The patient's 2D-ECHO showed diastolic dysfunction and also LVH , MR and TR with PAH.
Heart failure with preserved ejection fraction (HFpEF) happens when the left ventricle is not filling with blood as well as normal. The ventricle can pump well. But it may be stiff so it cannot relax and fill with blood as well as normal. The ejection fraction is 50% or more. HFpEF may also be diagnosed if the ejection fraction is 40% to 49%.
HFpEF happens because the left ventricle's muscle becomes too stiff or thickened. To compensate for stiff heart muscle, your heart has to increase the pressure inside the ventricle to properly fill the ventricle. Over time, this increased filling causes blood to build up inside the left atrium and eventually into the lungs, which leads to fluid congestion and the symptoms of heart failure
2.what is the reason for anaemia in this case?
ANS)
The patient has diabetic triopathy which means he showed, first, clinical evidence of neuropathy; then, diabetic retinitis, and, finally, the nephropathy of diabetes. Anemia can be due to decrease in erythropoietin production by the kidneys due to nephropathy which is usually common in patients with heart failure or it could be Anemia of chronic disease
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
ANS) Diabetic bullae, also known as bullosis diabeticorum, is a spontaneous, distinct, non-inflammatory, blistering condition of the skin predominantly seen in patients with diabetes mellitus.
Circulation of blood at the wound site is critical for wound healing. As a result of narrowed blood vessels, diabetic wound healing is impaired because less oxygen can reach the wound and the tissues do not heal as quickly.
4. What sequence of stages of diabetes has been noted in this patient?
ANS) The patient showed sequence of neuropathy followed by retinopathy and nephropathy
It is termed as DIABETIC TRIOPATHY.
C) Link to patient details:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS) According to the investigations that were done, it seems that the anatomical location are the atria (ASD) of the patient as they showed decreased intensity of contraction as a result of dilatation leading to stasis of blood in the atria forming thrombi. This could be the primary etiology of the patient’s problem.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS) Past-
10yrs ago - Operation for Hernia
Since 2-3 yrs - Facial puffiness
1 yr ago - SOB grade II
1 yr ago - was diagnosed with Hypertension.
When the patient came to OPD -
Since 2 days - SOB which progressed from Grade II to Grade IV.
Since 2 days - Decreased urine output.
Since 1 day - Anuria
After admission -
CT scan - Showed dilated pulmonary vessels and thrombi in the atria.
2D Echo - Showed LV dysfunction.
Anatomical location - Atria (SA node)
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
ANS) Cardiorenal syndrome encompasses a spectrum of disorders involving both the heart and kidneys in which acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. The patient showed Type 4 CRS - CKD resulting in chronic HF. It summarizes cardiac-kidney interactions in special populations such as patients with diabetes mellitus and kidney transplant recipients, and emphasizes the role of palliative care in patients with cardiorenal syndrome.
4) What are the risk factors for atherosclerosis in this patient?
Hypertension
Alcohol
5) Why was the patient asked to get those APTT, INR tests for review?
ANS) The patient showed Left atrial thrombi and LAA thrombi which could embolize and cause arterial obstruction elsewhere or can also cause stroke. This means that the patient is under the risk of developing thrombi or embolization of the existing ones. These tests will assess the platelet and clotting pathway function. Hence, they should be monitored.
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?
ANS) The patient is a diabetic from 12 years. His glucose levels at the time of admission were high which show that it was uncontrolled. Diabetes is a major risk factor for the development of ACS/ NSTEMI. It is a proatherosclerotic, proinflammatory, and prothrombotic stateAlso, the patient is a hypertensive , which is also a risk factor for ACS , but it was controlled. ACS is a mismatch in the myocardial oxygen demand and myocardial oxygen consumption . The patient showed coronary artery block that led to ACS.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS) The patient was given selective long acting beta-blocker METOPROLOL
Oral metoprolol is the most commonly prescribed β-receptor blocker in patients with ACS.
They reduce the complications of ACS lik re-infarction and total mortality.
Beta blockers work by reduction of oxygen consumption of the myocardium by lowering the heart rate, blood pressure, and myocardial contractility.
Based on recent evidence from the era of percutaneous coronary intervention, with the exception of the data from the J-Cypher registry in less than 1000 patients, other clinical trials that evaluated the prescription of oral beta blockers on discharge from hospital after acute coronary syndrome have demonstrated a prognostic benefit in total mortality with this medication, including in the subgroup of patients with preserved left ventricular systolic function.
3) What are the indications and contraindications for PCI?
INDICATIONS:
CONTRAINDICATIONS:
Intolerance for oral anti platelets 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.
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?
ANS) The complications may include bleeding, blood vessel damage, a treatable allergic reaction to the contrast dye, the need for emergency coronary artery bypass grafting during the procedure, arrhythmias, damaged arteries, kidney damage, heart attack, stroke, or blood clots. Sometimes chest pain can occur during PCI because the balloon briefly blocks blood supply to the heart. Restenosis, or tissue regrowth in the treated portion of the artery, may occur in the following months and cause the artery to become narrow or blocked again. The risk of complications is higher if you the patient older, have chronic kidney disease, are experiencing heart failure at the time of the procedure, or have extensive heart disease and multiple blockages in coronary arteries.
Research on overtesting and overtreatment important because the patient should not end up in iatrogenic problems as well financial problems.
Whatever needed has to be definitely done by taking the patient's consent but only after all the complications and the consequences have been taken into consideration.
E) 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?
Ans) First patient developed dragging type chest pain and was radiating to his back then he developed giddiness and chest pain. As the character of pain is dragging type and radiating and not burning type we can localise it to heart. On investigation it was found to be an inferior wall mi. Patient is diabetic and has also has hypertension could have lead to endothelial injury which lead to thrombus formation and occlusion leading to MI
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans) Aspirin has anti platelet effect and also an analgesic
Atorvastatin decreases the cholesterol levels
Clopidogrel has anti platelet effects and prevents further aggregation
Insulin has hypo glycemic effect and used as an emergency intervention in this patient
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans) Per cutaneous intervention(pci) or stunt placement was not a better option in this patient because it was done after 3 days of the symptoms onset and stent has its own complications of rethrombosis. Ideally it should be done before 12 hrs of onset of symptoms
F) Link to patient details:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
ANS) as patient was in initial stage of cardiogenie shock iv fluids might have helped the hypotension and have have increased venous return and perfusion to lungs. Hence momentarily subsided his breathlessness
2. What is the rationale of using torsemide in this patient?
ANS) Torasemide is a diuretic. As the patients urine output is low and there is increase burden on heart as it is not pumping out blood which might increase the back pressure and may cause edema or fluid escaping into third space. So to prevent it patient might’ve been given torasemide and also to increase urine output.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
ANS) Giving Ceftrioxone was probably to treat UTI as patient had history of whitish discharge.
4) Gastroenterology (& Pulmonology)
A) 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.
Ans) The anatomical location of patient's problem is the PANCREAS
5 years ago - He developed pancreatitis which was treated conservatively.
He then stopped alcohol and everything was fine till 3 years
later, he started taking toddy since 2 years during which he 4-5 developed episodes of abdominal pain and vomitings. He still continued to consume toddy which led to following problems and the sudden presentation as mentioned in the case above.
The cause of pancreatitis here may be attributed to alcohol ( primary etiology); In acute pancreatitis, there is premature activation of zymogen granules in pancreas leading to increased release of proteases into surrounding tissues. Acute pancreatitis is often self limiting condition but in some patients with severe disease or frequent recurrent episodes of acute pancreatitis; like in this case is associated with complications like pseudocyst formation, necrosis etc.., And also systemic complications. Following an inflammatory rupture of pancreatic duct, a collection of fluid & debris may develop in lesser sac known as pancreatic fluid collection. Initially it has poorly developed fragile granulation tissue wall which after 6 weeks developed into a fibrous capsule and forms PSEUDOCYST. CE CT is a confirmatory test here and most important in diagnosis as it will also show the local complications and other supportive investigations like : CBP , LFT, serum amylase , pleural fluid analysis
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
Ans) TREATMENT along with mechanism of action:
1) ING. MEROPENAM ; TID for 7 days -Meropenem ( broad spectrum Carbepenem ) an antibiotic.
2) ING. METROGYL 500 mg IV TID for 5 days - inj. Metrogyl has METRONIDAZOLe - ( Nitroimidazole drug ) an antibiotic
3) ING. AMIKACIN 500 mg IV BD for 5days - It is an Aminoglycoside antibiotic
## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.
4) TPN ( Total Parenteral Nutrition )
* Method of feeding that by passes gastrointestinal tract. Fluids are given to vein , it provides most of the nutrients body needs. TPN has proteins, carbohydrates, fats, vitamins, minerals.
5) IV NS / RL at the rate 12l ml per hour- Given for fluid replacement ie., treat dehydration
6) ING. OCTREOTIDE 100 mg SC , BD - It is a Somatostatin long acting analogue. It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.
7) ING. PANTOP 40 mg IV , OD - Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.
8) ING. THIAMINE 100 mg in 100 ml NS IV , TID
* It is B1 supplement. It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency .Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.
9) ING. TRAMADOL in 100 ml NS IV , OD - It is an opioid analgesic, given to releive pain
## After 4 days of this treatment; there is no improvement in patient and infact he is deteriorating clinically.
* So USG GUIDED MALECOT DRAIN - PLACED INSIDE AND PSEUDOCYST WAS DRAINED
* TWO OTHER USG GUIDED DRAINS ARE PLACED TO DRAIN THE PERI-PANCREATIC COLLECTIONS
## After this patient was dramatically improved but in the mean time he developed PNEUMOTHORAX IN LEFT LUNG
* Oxygen supply for mild hypoxia
* And ICD ( Inter Coastal Drain ) was placed to relieve the pneumothorax.
B) Link to patient details:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
Ans) The patient developed pleural effusion which is the reason for his dyspnea.
It is related to pancreatitis as when a patient develops acute pancreatitis , the pancreas releases a lot of enzymes and fluid leading to fluid collection in the nearby areas which begin in the peritonuim and slowly diffuse into the thoracic side of diaphgram , i.e., into the pleura. This is also the reason for the patient ascites. Pleural effusion is considered to be the marker of acute pancreatitis and now a days it is considered to be the marker for severity and mortality indicator for the disease.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
ANS) *Disorders of the exocrine pancreas including pancreatitis and pancreatic cancer can lead to endocrine dysfunction and abnormal glucose metabolism .The criteria to define AP severity include the presence and extent of pancreatic necrosis which reflects the pancreas local situation, and aspects of system organ dysfunction. Tu et al. (2017) reported that AP patients with pancreatic necrosis had much higher incidence of DM later on compared to those who had no pancreatic necrosis.
( De novo type 2 Diabetes Mellitus)
* Maybe the patient was a unknown case of diabetes.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
ANS) * The patient also had FATTY LIVER. This could be the cause of elevated LFT
* Specific marker for ALC.FATTY LIVER - γ-Glutamyl transpeptidase (GGT) - considered to be more sensitive. Also, Typical laboratory findings in ALD include transaminase levels with aspartate aminotransferase greater than alanine aminotransferase as well as increased mean corpuscular volume, and IgA to IgG ratio. It should always be supported by imaging or biopsy techniques.
4) What is the line of treatment in this patient?
Treatment:
• IVF: 125 mL/hr- For dehydration and fluid balance.
• Inj PAN 40mg i.v OD- PPI
• Inj ZOFER 4mg i.v sos - Anti emetic
• Inj Tramadol 1 amp in 100 mL NS, i.v sos - Analgesic
• Tab Dolo 650mg sos - Analgesic
• GRBS charting 6th hourly • BP charting 8th hourly
C) Link to patient details:
Possible Questions :-
1) what is the most probable diagnosis in this patient?
ANS) Hemoperitoneum could be the probably diagnosis as there is evidence of fluid and hypotension indicating hemorrhagic shock.
2) What was the cause of her death?
ANS) Cause of her death could be due to haemorrhage or due to massive blood transfusion of her lung injury or hepatic encephalopathy or any complication during lapro
3) Does her NSAID abuse have something to do with her condition? How?
ANS) NSAIDS on long term use are hepatotoxic so might have aggregated the cause
5) Nephrology (and Urology)
A) Link to patient details:
1. What could be the reason for his SOB ?
ANS) High creatinine in the serum might be the cause of SOB.
2. Why does he have intermittent episodes of drowsiness ?
ANS) Could be as a result of UTI in the patient as a result of fatigue which is usually associated with it.
3. Why did he complaint of fleshy mass like passage in his urine?
ANS) The urine was composed of pus cells, making it thicker than usual, so ,the patient might have felt it to be a fleshy mass.
4. What are the complications of TURP that he may have had?
ANS)URINARY TRACT INFECTION
B) Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
ANS) It could lack of proper behavior training or could be Attention Deficit Hyperactivity Disorder (ADHD) could be the cause
2. Why doesn't the child have the excessive urge of urination at night time ?
ANS) There can be a chance of the manifestation being psychosomatic, or as a result of an undiagnosed anxiety disorder, or a stressor triggering this manifestation.
3. How would you want to manage the patient to relieve him of his symptoms?
ANS) A placebo can be tried , for example, MVT to rule out psychosomatic illness.
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
A) Link to patient details:
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
ANS). History of coughing after taking food since 2 months ,as the food through fistula had passed into trachea and stimulated the cough receptors. On barium swallow there is leakage of contrast into left bronchi.
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
ANS) There is very less chance that patient might be developing immune reconstitution inflammatory syndrome as the CD4 counts were not very less during the start of treatment. Could be due to TB or any opportunistic infections or neoplasm
7) Infectious disease and Hepatology:
Link to patient details:
1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?
ANS) YES , 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)
ANS) Reasons for this association between local alcohol beverages and ALA could be multifactorial. Factors influencing the association could be related to the pathogen, contents of beverages, status of the liver, and the immunity of the host. They are more vulnerable perhaps due to the large infective dose of Entamoeba histolytica and other bacterial pathogens ingested with the unhygienically brewed beverage. Associated nutritional status of the population and poor sanitation could also play a pivotal role. Hai et al. stated that alcohol-induced hepatic dysfunction and possible suppression of amoebistatic immune mechanisms by substances in the beverages could also be attributed in the mechanism
Mukhopadhyay et al. have suggested that “alcohol can predispose to ALA through a multitude of mechanisms, including 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 ?
ANS) YES, it is more common in the right lobe as it occupies significant part of the liver as well as receives as good as 50% of the blood supply.
4.What are the indications for ultrasound guided aspiration of liver abscess ?
ANS) Indications
- complicated diverticular abscess.
- Crohn's disease related abscess.
- complicated appendicitis with appendicular abscess.
- tuboovarian abscess.
- post-surgical fluid collections.
- hepatic abscess (e.g. amoebic or post-operative)
- renal abscess or retroperitoneal abscess.
- splenic abscess.
B) Link to patient details:
QUESTIONS:
1) Cause of liver abscess in this patient ?
ANS) Local toddy which might have been contaminated with E. hystolytica or with any other bacteria.
2) How do you approach this patient ?
ANS) The patient has to be first examined physically, tenderness in the right hypochondrium is a slient feature. then, management of the patient includes investigations like CBP, CUE LFT, Stool examination and antigen detection Imaging- Chest X-RAY, USG , CT and MRI can also be done as they're highly sensitive. After the provisional diagnosis following treatment has to be given and regular USG has to be done as a follow up to monitor the abscess.
* INJECTION. ZOSTUM 1.5 gm IV BD (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)
* INJECTION. METROGYL 500mg IV TID ( thrice daily )
Metrogyl has the drug called METRONIDAZOLE [Antibiotic]: For amoebic cause
* INJECTION. OPTINEURIN 1amp in 100 ml NS( Nor
mal Saline) IV OD ( once daily)
Optineurin is a multivitamin drug { A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement
* TAB. ULTRACET 1/2 QID( four times a day)
Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and fever
* TAB. DOLO 650 mg SOS (if needed) given for fever and pain
3) Why do we treat here ; both amoebic and pyogenic liver abscess?
ANS) It is rarely possible to differentiate between amoebic liver abscess and bacterial liver abscess just by imaging and stool examination . Hence, whenever there is a case of liver abscess it is treated for both pyogenic and amoebic liver abscess until and unless there is a definitive diagnosis of either of them as risk cannot be taken.
4) Is there a way to confirm the definitive diagnosis in this patient?
ANS) The diagnosis of amebic liver abscess was based on four or more of the following criteria: (i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess, (ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder), (iii) enlarged and/or tender liver, usually without jaundice, (iv) raised right dome of the diaphragm on chest radiograph, and (v) improvement after treatment with antiamoebic drugs (e.g., metronidazole).
It's always made by following the above criteria. But, according to some studies , ANTIGEN detection and PCR have proven to be sensitive and confirmative for Amoebic liver abscess.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
A) 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?
ANS) The patient was a chronic diabetic and hypertensive which lead to ketoacidosis and secondary fungal infection. The primary etiology here is uncontrolled diabetes.
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
ANS) Insulin administration is essential in DKA treatment because it promotes glucose utilization by peripheral tissues, diminishes glycogenolysis and gluconeogenesis, and suppresses ketogenesis. Intravenous infusion is a preferred route of insulin delivery in patients with DKA.13 Insulin infusion without initial volume resuscitation is not advised as it may only worsen dehydration. An initial bolus of regular insulin of 0.1 U/kg followed by continuous insulin infusion is usually done.
DKA in dialysis patients may differ in the clinical and laboratory presentation and the treatment, compared with DKA in non-dialysis patients.
Reduced glomerular filtration rate, insulinopenia, and hypertonicity result in positive potassium balance, placing ESKD patients with DKA at high risk for hyperkalemia. Hyperkalemia is typically more severe in dialysis patients compared with non-dialysis patients for the same levels of hyperglycemia and can be life threatening. Consequently, routine potassium replacement is not indicated unless plasma potassium level is below 3.3 mmol/L. Insulin is typically the only treatment necessary for hyperkalemia in dialysis-dependent patients with DKA. Severe hyperkalemia requires electrocardiographic monitoring for signs of cardiac toxicity. Potassium measurement level should be repeated 2 hours post-procedure to monitor for its intracellular rebound after hemodialysis.
Management of acute kidney injury involves fluid resuscitation, avoidance of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances. Renal replacement therapy (dialysis) is indicated for refractory hyperkalemia; volume overload; intractable acidosis; uremic encephalopathy, pericarditis, or pleuritis; and removal of certain toxins. Recognition of risk factors (e.g., older age, sepsis, hypovolemia/shock, cardiac surgery, infusion of contrast agents, diabetes mellitus, preexisting chronic kidney disease, cardiac failure, liver failure) is important.
1.Injection Mannitol 100ml/IV/TD
Mannitol is an osmotic diuretic, typically used at 0.25–0.5 g/kg IV administered over 15 minutes. It lowers intracranial pressure
2.TAB Ecospirin 75 mg po/OD
Aspirin irreversibly inhibits cyclooxygenase, which prevents the conversion of arachidonic acid to thromboxane A2 (TXA2). Thromboxane A2 is a vasoconstrictor and stimulator of platelet aggregration. Platelets are inhibited for their full life cycle (5–7 days) after exposure to aspirin. Aspirin also inhibits prostacyclin activity and this inhibits platelet aggregration. The effects of aspirin on prostacyclin are dose related.
3.TAB ATORVAS 40mg po/HS - To lower cholesterol levels.
4.BP/PR/TEMP/SP02 MONITORING (4th hourly)
Maintaining adequate tissue oxygenation is important during periods of acute cerebral ischemia in order to prevent hypoxia and potential worsening of the neurologic injury. Supplemental oxygen should be administered if there is evidence of hypoxia by blood gas determination or desaturation detected by pulse oximetry.
Treatment of orbital cellulitis includes antibiotics and other supportive therapies. An ophthalmologist and otolaryngologist should also be consulted for proper examination and because, in some cases, surgery may be required. The choice of antibiotics is broad spectrum regimens aimed at covering for organisms such as S. aureus (including methicillin-resistant S. aureus [MRSA]), Streptococcus pneumoniae, other Streptococci, as well as gram-negative bacilli.
ANTIFUNGAL - AMPHOTERICIN -B for MUCORMYCOSIS
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
ANS) So far, this surge has been attributed to the improper use of steroids to treat Covid-19 patients, coupled with poorly managed diabetes. But steroids in themselves are not the villains.
9) Infectious Disease (Covid 19)
Covid 19 with co morbidity (Pulmonology/Rheumatology)
1) How does the pre-existing ILD determine the prognosis of this patient?
\ANS: Patients with ILD already have a poor lung reserve and reduced gaseous exchange and their oxygen saturation’s are less. They have less viable lung tissue. On top of that COVID caused lung endothelial damage and further decrease satuarions. Patient may also develop pulmonary artery hypertension with chronic hypoxia. So patient may develop complications at a low threshold. Studies have shown that there’s high mortality in patients with ILD and severe COVID . As the patient seems to be moderately effected by COVID complications could be less. SARS-CoV-2 infects cells with ACE2 as a receptor, and the reduced infection rate of COVID-19 in patients with ILD has been proposed to be due to decreased angiotensin II mRNA activity in the lung in ILD. This same study stated that although the risk of infection might be lower in patients with ILD, once infected, the severity and prognosis are worse in patients with ILD due to aggravated inflammatory responses and coagulopathy.
2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism?
ANS: Steroids given for COVID doesn’t effect rheumatoid arthritis as it one of the medication for rheumatoid arthritis. While it can precipitate hypothyroidism as steroids prevent the peripheral conversion of T4 —> T3 and also decreases TSH production. So hypothyroidism could be precipitated.
3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?
ANS: given that there has been no increase in exacerbations of RA patients concomitantly suffering from COVID-19 and no increase in new cases during the pandemic so far. Theatrically it may be true but practical evidence is not yet established. SARS-CoV-2 may trigger autoimmunity phenomena associated with a state of transient immunodeficiency of components of both innate and acquired immunity in which the immune system fails to properly recognize of autoantigens. This is associated a form of immune reconstitution that would magnify this anomaly in the convalescence of the disease
4) Why was she prescribed clexane (enoxaparin)?
ANS : Acute inflammation promotes a hypercoagulable state that may increase the risk of deep vein thrombosis (DVT) and pulmonary embolism.In chronic inflammatory disease such as rheumatoid arthritis (RA), procoagulatory factors are up-regulated
2) Covid 19 with Diabetes
Link to the patient case report
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?
ANS: 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
This large burden of inflammatory cells can affect the functions of skeletal muscle and the liver, the major insulin-responsive organs that are responsible for the bulk of insulin-mediated glucose uptake.In addition, patients with severe COVID-19 show muscle weakness and elevation of liver enzyme activities, which might suggest multiple organ failure, particularly during a cytokine storm.
In individuals with obesity, pro-inflammatory cytokines with a T helper type 1 cell signature are known to increase insulin resistance.
The SARS-Cov-2 tropism for the β-cell could cause acute impairment of insulin secretion or destruction of β-cells resulting in de novo development of diabetes.
2) Did the patient's diabetic condition influence the progression of her pneumonia?
ANS: The airway surface liquid (ASL) plays a pivotal role in lung defense. Diabetes is related with higher ASL glucose concentration, ASL volume accumulation in alveolar space, imbalance of reactive oxidative species (ROS), and inflammatory chemokine production.
(2) The COVID-19 infection promotes injuries in type I and type II pneumocytes and lung endothelial lesions, with subsequent additional secretion of protein-rich exudate in the alveolar space and intravascular coagulation in lung vessel, which leads to a reduction in surfactant and gas exchange.
(3) The association between diabetes and SARS-CoV-2 increases the glucose and protein concentration in ASL, leading to increase the risk of pneumonia.
Bearing in mind the osmotic effect due to the high ASL glucose concentration, these changes could explain the higher total water content in lung during hyperglycemic condition, which can be related with higher volume of ASL, leading to reduced gas exchange rates of O2 and CO2 between alveolar space and lung capillaries. Frequently, the mild increase in ASL can be compensated by ventilatory response mechanisms. It is important to point out that the pathological reduction of O2 and CO2 exchange through the lumen of pneumocytes and blood occurs in poorly controlled diabetic patients mainly under bacterial, inflammatory, or oxidant disruptions.
The high concentration of glucose and the increased volume in the ASL are maintained mainly by the low expression of SGLT1 in the apical membrane of type I and II pneumocytes in the lungs of diabetics. Hyperglycemia promotes increased paracellular glucose transport from blood to ASL. The evolution of DM promotes activation of the inflammatory cascade with the production of interleukins, increased ROS, and endothelial damage. These changes provide an increased risk for pneumonia due to the proliferation of bacteria P. aeruginosa and MRSA.
3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?
Ans: elevated baseline D-dimer levels are associated with inflammation but not with VTE score in COVID-19 patients, suggesting that it is unreasonable to judge whether anticoagulation is needed only according to D-dimer levels. However, the abnormal changes of D-dimer and inflammatory factors suggest that anticoagulant therapy might be needed.
3) Covid 19 Severe
Link to the complete case report log:
Questions:
1. Why was this patient given noradrenaline?
ANS) In hypotensive vasodilated patients with acute kidney injury, restoration of blood pressure within autoregulatory values should occur promptly with noradrenaline and be sustained until such vasodilatation dissipates.
2. What is the reason behind testing for LDH levels in this patient?
ANS) High levels of LDH indicate some form of tissue damage. High levels of more than one isoenzyme may indicate more than one cause of tissue damage. Serum LDH is an appropriate and cost-effective prognostic indicator that can be used for risk classification of patients at risk for rhabdomyolysis-induced AKI.
3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
ANS) The patient had developed AKI along with hypotension and tachycardia, associated with a feeble pulse and altered sensorium.
The main benefits of mechanical ventilation are the following:
- 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 Link to the case report log:
Questions:
1. Is the elevated esr due to covid related inflammation?
ANS) COVID-19 might trigger the change of the form of erythrocytes or plasma characteristics including the immune system via an unknown mechanism to increase the ESR. It is however a prognostic factor for Covid-19 infection.
2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization?
ANS) The patient got admitted because even after home isolation for 14 days, his test came positive and further he experienced symptoms of fever, fatigue and loss of taste and smell.
Getting admitted to hospital might lead to nosocomial infections and hence home isolation is advised for MILD COVID patients.
Though, the mild covid patients are advised for home isolation, the patient has to follow all the guidelines to prevent worsening of the disease such as:
- Should stay in a separate well ventilated room. It is preferable to have a separate toilet.
- Keep yourselves hydrated. Drink atleast 2 liters of water per day. Use boiled and cooled water for drinking.
- Maintain isolation. Always wear a mask, should you step out of your room in unavoidable circumstances.
- Always use handkerchief / tissue and cover your mouth while coughing or sneezing. The used handkerchief should be stored in airtight polythene cover till washing.
- Used tissue shall be disposed along with used masks in a closed dustbin with secure lid.
- Burn the used masks & tissues to ashes outside your home. Do not dispose it with other household trash.
- Always use a handkerchief or tissue. If the handkerchief becomes wet or soiled, put it in a polythene cover. If you use tissue papers dispose them in a trash can that has a lid.
- Always wash your hands with soap and water for 40 to 60 seconds before using the toilet. Do not use cloth for wiping wetness. It is advisable to raise your hand and allow it to air dry.
- After using the toilet, clean all the surfaces that you have touched and wash your hands with soap and water.
- The patient should clean the isolation room himself/herself. If that is not possible the person who is cleaning should take all necessary precautions like wearing triple layer medical mask, gloves, face shield/ goggles.
- The room should be cleaned with disinfectants (as per manufacturer guidelines) or bleaching powder mixed with water (3 spoons per litre) twice a day.
- Always maintain a distance of 2 meters (i.e. 6 feet) with senior citizens, pregnant women, children and comorbid patients at home.
THESE GUIDELINES HAVE BEEN PROVIDED BY GOVERNMENT.
5) Covid 19 and comorbidity (Altered sensorium, azotemia, hypokalemia)
Link to the case report log:
Questions:
1) What was the reason for coma in this patient?
ANS) It could be due to hypoxic brain injury. The patient's ABG report also showed high pCO2 levels.
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?
ANS) It may have been due to lack of diagnostic tests in the previous hospitals. The diagnosis of hypokalemic PP should be done with Genetic testing and Analysis which is confirmatory.
Supportive diagnostic criteria for HypoPP
|
ANS) Covid -19 patients with severe disease leading to respiratory failure and hypoxic/ anoxic brain injury tend to end up in coma.
6) Severe Covid 19 with altered sensorium
Link to the case report log:
1. What was the cause of his altered sensorium?
ANS) Could be due to constant hypoxia or uraemic encephalopathy or any toxins induced as patients liver is injured
2. What was the cause of death in this patient?
ANS) Could be due to micro thrombosis effecting multiple organs especially brain clots.
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