"This is my submission for the Bimonthly internal assessment for the month of November."
Most of the information here have been collected from different reference sites, the links to which have been mentioned. The points copy pasted have been put in quotes.
The questions to the cases being discussed can be viewed from the link below 👇
https://medicinedepartment.blogspot.com/2020/11/blended-learning-bimonthly-assignment.html?m=1
Some of these were collected from Harrison's principle of Internal Medicine and the links shared :)
55 year old male patient came with the complaints of
Chest pain since 3 days
Abdominal distension since 3 days
Abdominal pain since 3 days and decreased urine output since 3days and not passed stools since 3days
https://sreejaboga.blogspot.com/2020/11/is-online-e-log-book-to-discuss-our.html?m=1
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
The first case presented to us is that of a
55 year old man obese patient, who has been an alcoholic and smoker since 30 years presented to us with
Pain in the epigastrium since 3 days
Abdominal pain and distension since 3 days
Unable to pass stools since 3 days
and reduced urine output since 3 days
Dyspnea since 3 days
A. ANATOMICAL LOCATION OF THE PATIENTS PROBLEM:
From the history, this i what i analyze
Pain in the epigastrium could be because of Myocardial infarction, Peptic Ulcer, Gastritis, Pancreatitis
Abdominal distension could be because of Ascites
Unable to pass stool could be because of intestinal obstruction, paralytic ileus
Reduced urine output could be because of kidney injury, obstructive uropathy
Dyspnea could be due to acute lung injury, renal failure due to fluid overload or intestinal obstruction
B. ANATOMICAL AND ETIOLOGICAL WORK UP
From his investigations i can see that his Serum Amylase is elevated and his USG Abdomen shows Acute Pancreatitis with Multiple Gallbladder calculi and Minimal Ascites - explaining the cause for pain abdomen and abdominal distension being pancreatitis.
From the history, i can see multiple factors that have contributed for him to have acute pancreatitis such as:
-Gallstones being the leading cause of pancreatitis
-Alcoholism (the second most common cause of pancreatitis)
Hyper triglyceridemia, Smoking
-Age (55 years)
RFT shows erum creatinine of 150 mg/dl and Blood urea of 150 mg/dl along with hypocalcemia and he also complains of reduced urine output explaining Renal failure secondary to acute severe pancreatitis
His ABG shows metabolic acidosis - ?Renal failure induced
His Chest xray shows minimal bilateral pleural effusion with bilateral infiltrates - Acute lung injury
Pleural effusion and ascites could be due to third space fluid loss.
From the history, i can see multiple factors that have contributed for him to have acute pancreatitis such as:
-Gallstones being the leading cause of pancreatitis
-Alcoholism (the second most common cause of pancreatitis)
Hyper triglyceridemia, Smoking
-Age (55 years)
-Acute severe pancreatitis could lead to Multiorgan damage involving the lungs,kidneys
This patient's acute severe pancreatitis lead him to acute kidney injury and acute lung injury
Unable to pass stools could be due to - Hypoperfusion or ischaemia, intestinal impaired mucosal barrier, Antibiotic induced bacterial overgrowth.
Lets discuss about the pathogenesis involved in acute pancreatitis
https://www.researchgate.net/figure/Schematic-overview-of-pathogenesis-of-acute-pancreatitis-Acinar-cell-damage-leads-to_fig1_280741425
Autodigestion theory states that
Proteolytic enzymes such as Trypsinogen gets activated into trypsin along with other proteolytic enzymes leading to disgestion of the pancreatic tissue, peri pancreatic tissue and further release of other enzymes such as Elastase, phospholipase A2
The pathogenesis involved in Acute pancreatitis involves 3 stages:
1. The cellular phase
First phase involves the damage of the acinar cells, due to alcoholism, hyperlipidemia or any other toxins causing activation of trypsinogen and release of various cytokines and inflammatory mediators ----> Lysosomal hydrolase such as Cathepsin B becomes colocalized with digestive enzymes in intracellular organelles which further activate Trypsin --> Acinar cell injury
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1742-7843.2005.pto_274.x
2. The inflammatory response
It involves the activation,chemo attraction, sequestation of leukoocytes and macrophages in the pancreas. Neutrophils can apparently activate trypsinogen continuing the cycle of inflammation.
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1742-7843.2005.pto_274.x
3. The Third phase - is Systemic inflammation
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1742-7843.2005.pto_274.x
The inflammed pancreas release Proteolytic enzymes and cytokines which further effect the distant organs.
Trypsin activation leads to pancreatic tissue digestion + peripancreatic tissue digestion + activation of other enzymes such as Phospholipase A2, Elastase. The activated enzymes + cytokines digest cellular membranes leading to ----> Proteolysis, Edema, Interstitial Hemorrhage, Coagulation necrosis, fat necrosis, Parenchymal cell necrosis.
Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
a1) Added 17/11/2020 Mention the optimal diagnostic interventions in the patient done and that you may further order in a low resource setting to fathom the etiologic possibilities
Routines such as hemogram to look for sepsis, RFT to assess the serum creatinine and blood urea levels as the patient was in renal failure, ABG shows metabolic acidosis due to renal failure
FLP shows hypertriglyceridemia
USG Abdomen to look for the cause of abdominal pain
Thyroid profile wouldn't really be helpful in ICU patients would be misleading as Low fT3 level was the most common abnormality found in these patients. High TSH and low fT4.
https://www.biomedres.info/biomedical-research/assessment-of-thyroid-function-in-critically-ill-patients.html
Right upper limb carotid doppler was done as the patient had right upper limb venous stasis and had feeble pulse which revealed complete occlusion of right radial & ulnar artery, and right distal large plaque extending to proximal ICA causing 50-70% stenosis
I would further order for a CECT ABDOMEN to look for the CT severity index. CT abdomen would've helped to look for pancreatic necrosis, any calcifications or cysts.
b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
Pharmacological interventions :
1. Adequate fluid resuscitation needs to be performed the first 24-48 hours followed by high volume fluid therapy of 1000ml/hour
2. Giving antibiotics such as INJ PIPTAZ AND INJ METROGYL in this patient is questionable.INJ
Antibiotics haven't been proven to be efficacious in patients with acute pancreatitis as its an inflammatory process. ` `
Here is an interesting article i found
P - 1097 with Severe Acute Panceatitis who were admitted to the study institutions between January 1, 2009, and December 31, 2013, a retrospective cohort study of all consecutive patients.
I- Of the 1097 patients with SAP, 850 (77.5%) received antimicrobial prophylaxis, and 21 (1.9%) had invasive pancreatic candidiasis.
O-In multivariable logistic regression analysis, antimicrobial prophylaxis was significantly associated with the development of invasive pancreatic candidiasis.
The results suggest that antimicrobial prophylaxis may contribute to the development of invasive pancreatic candidiasis, and therefore, the routine use of antimicrobial prophylaxis for SAP may be discouraged
However, from Day 5 total leucocyte count has elevated probably due to line induced sepsis, starting him on an antibiotic Vancomycin would be suggestible.
3. INJ TRAMADOL was given for relieve patients pain
4. INJ LASIX was given as the patient was in fluid overload
5. NEBULIZATION WITH BUDECORT as the patient had Acute lung injury, as it has anti inflammatory effect an reduces pulmonary edema and improves patients oxygenation.
Non Pharmocological interventions:
Nil per oral - as food intake would stimulate pancreatic enzyme secretion in an inflammed pancreas.
Here's an article on Nasogastric feed versus NPO in acute pancreatitis
P- 35 patients with acute pancreatitis were randomised and compared regarding early nasogastric tube feeding versus nil per oral
I- There were 17 patients randomly allocated to the NGT group.
C- 18 to the NPO group.
O-The number of patients not requiring opiates at 48 h after randomization was significantly different between NGT (9/17) and NPO (3/18). Oral food intolerance was observed in 1/17 patient in the NGT group and 9/18 patients in the NPO group. The overall hospital stay in the NGT group was 9 (5-12) days as compared with 8.5 (6-13) days in the NPO group.
NGT commenced within 24 h of hospital admission is well tolerated in patients with mild to moderate acute pancreatitis. Further, when compared with NPO, it significantly reduces the intensity and duration of abdominal pain, need for opiates, and risk of oral food intolerance, but not overall hospital stay.
Another article which states that there were no significant different on started patients on oral feeds immediately against keeping them Nil Per Oral
However since our patient had severe acute pancreatitis, NPO would be preferred.
2) A 55 year old male, shepherd by occupation, presented to the OPD with the chief complaints of fever (on and off), loss of appetite, headache, body pains, generalized weakness since 2 months, cough since 2 weeks and vomitings and pain abdomen since 2 days.
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
Patient is anemic, with renal failure, the renal function test shows elevated serum creatinine and blood urea with elevated correct calcium of 9.2 mg/dl, hyperphosphotemia, LFT shows gamma gap as high as 6.7, his esr is elevated, X-ray skull shows lytic lesions.
1. ANATOMICAL LOCATION:
1.The anatomical location is the bone marrow. Multiple Myeloma represents malignant proliferation of plasma cells derived from a single clone.
2. Bone Pain - Occurs due to proliferation of tumors cells, increased osteoclastic activity and reduced osteoblastic activity.
3. Anemia - Expanding tumor in the bone marrow, decreased erythropoeitin production, inhibition of hematopoeisis by tumor factors and also vitamin B12 and folic acid deficiency contributes to anemia in MM.
Antibody coated platelets could lead to thrombocytopenia.
4. Headache - could be due to hyperviscosity which occurs due Hyperviscosity.
If M component froms cryoglobulins.
Clotting abnormalities could occur due to interactiong between 1,11,V,V11,V111 and antibody coated platelets or amyloid damage to the endothelium.
5. Right upper and middle lobe consolidation with right sided pleural effusion. Patients with Multiple Myeloma are prone to recurrent infections. Sputum for CBNAAT is positive suggesting Pulmonary
Koch's.
These patients are prone to infections as they are immunocompromised.
6. Renal Failure - could be due to hypercalcemia, Glomerular deposits of amyloid, hyperuricemia, recurrent infections, frequent use of NSAIDS. Normally light chains are reabsorbed in the tubules, and catabolized. With the increase of light chains in the tubules, tubular ces become overloaded with these proteins, tubular damage directly due to light chains or by the release of lysozomal enzymes.
Fanconi's syndrome ( proximal RTA ) is the earliest manifestation.
The cause is not known. But have been reported more in persons exposed to radiation and among farmers, wood workers, leather workers, petroleum products. N-ras,K-ras, B- raf mutations have been reported most commonly. IL-6 may play a role in myeloma disease progression.
PATHOGENESIS OF THESE SYMPTOMS:
Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
DIAGNOSTIC CRITERIA
From the Harrison's Principles of Internal Medicine
From the Harrison's Principles of Internal Medicine
From the Harrison's Principles of Internal Medicine
b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
1 PRBC transfusion was done for anemia.
APPROACH TO MULTIPLE MYELOMA FROM HARRISON'S PRINCIPLE'S OF INTERNAL MEDICINE
A double-blind, placebo-controlled trial, patients with untreated symptomatic MM were randomized to thal/dex or to placebo plus dexamethasone
P - A total of 470 patients were enrolled
I - Patients in arm A received thalidomide 50 mg orally daily, escalated to 100 mg on day 15, and to 200 mg from day 1 of cycle 2; dexamethasone 40 mg was administered orally on days 1 through 4, 9 through 12, and 17 through 20 during cycles 1 through 4 and on day 1 through 4 only beginning with cycle 5.
C - Patients in arm B received placebo (identical to thalidomide administration) and dexamethasone was administered as in arm A.
Cycles were 28 days long, and were repeated until progression or undue toxicity; there was no gap between cycles
O - Response to therapy with thal/dex was rapid, with a median time to response of 1.9 months compared with 4.6 months for placebo/dex (P < .001). Disease progression within the first 4 cycles of therapy was noted in 9.8% of patients receiving thal/dex and 14.0% of patients receiving dex alone
Thal/dex results in significantly higher response rates and significantly prolongs TTP compared with dexamethasone alone in patients with newly diagnosed MM.
COMPARATIVE EFFECTIVENESS OF THALIDOMIDE AND LENOLIDOMIDE IN MULTIPLE MYELOMA
P- Our cohort included 1264 myeloma patients who initiated either thalidomide or lenalidomide.
I- 406 used Thalidomide
C- 858 used lenolidomide
O- Among 406 new users of thalidomide, 142 (35%) developed peripheral neuropathy during a mean 499 person-days of follow-up. Among 858 new users of lenalidomide, 244 (29%) developed neuropathy during 587 person-days. Compared with thalidomide initiators, lenalidomide initiators had a reduced risk of peripheral neuropathy. We found no difference in rates of death.
Our results agree suggest that thalidomide and lenalidomide are equivalent with respect to survival outcomes but different with respect to neurotoxicity
A triple therapy is being recommended with - Dexamethasone + Thalidomide/Lenolidomide+ Bortezomib
Many side effects have been reported with Thalidomide so its suggested to use anticoagulants as a prophylaxis to DVT.
If Bortezomib is being administered, herpes zoster prophylaxis is recommended,
Supportive therapy for hypercalcemia such as Bisphosphonates, Hydration, erythropoeitin with hematinics could be given such as iron,folate,vitamin b12.
The last resort would be Stem cell transplantation.
3) 51 Year old man with complaints of B/L pitting pedal edema from 5 to 6months,abdominal distension from 2 to 3 days,SOB from 3days.
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
B/L pitting pedal edema from 5 to 6months, Abdominal distension from 2 to 3 days, Dyspnea from 3days.
Decreased urine output from 2 days
Known case of type 2 Diabetes Mellitus 7 years, hypertensive 5 years
History of 1 episode of seizures in 2017 and Atrial Fibrillation
A patient with Bilateral pedal edema, Abdominal distension, Dyspnea could be due to
1) Heart failure
2) Renal failure
3) Hypoalbuminaemia
1. Heart failure with reduced ejection fraction:
'Insulin resistance and DM are responsible for several functional, metabolic, and structural alterations that ultimately generate myocardial damage and HF progression. In particular, abnormalities in contractile proteins and impaired relaxation, change in substrate utilization, cellular injury, microvascular dysfunction, and neurohormonal and sympathetic nervous systems activation are main mechanisms HF patients.
Cardiac morphology appears also affected by obesity. Increased LV mass, usually associated to enlarged end-diastolic volume has been reported in obese normotensive subjects.
Adiponectin is the most abundant adipokine produced by fat tissue that has been demonstrated to exert anti-inflammatory and insulin-sensitizing actions, the latter through stimulation and activation of AMP-mediated protein kinase phosphorylation.
Obesity and DM are associated with reduced levels of adiponectin and type 1 and 2 adiponectin receptors, responsible for impaired insulin sensitivity and oxidative metabolism
in Hypertension, Mechanical stress due to increased pressure load together with high levels of neurohormones, cytokines, and growth factors induce development of concentric LV hypertrophy that can progress to symptomatic HF with either preserved or abnormal LV function'
https://academic.oup.com/eurheartj/article/36/39/2630/2398326https://academic.oup.com/eurheartj/article/36/39/2630/2398326
https://academic.oup.com/eurheartj/article/36/39/2630/2398326https://academic.oup.com/eurheartj/article/36/39/2630/2398326
Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
THERAPEUTIC APPROACH IN PATIENTS WITH HEART FAILURE
1. TAB MET XL
USE OF BETA BLOCKER IN HEART FAILURE:
Heart failure is accompanied by increase activation of sympathetic activity. This brings structural % functional modification in myocardium. Beta blockers inhibit the sympathetic outflow of norepinephrine and counteract the changes. The ventricular remodelling in heart failure is also reversed by beta blockers.
2. USE OF ENALAPRIL IN HEART FAILURE - Afterload reduction
Me and my colleague have previously discussed this article on Angiotensin - Neprilysin inhibition versus Enalapril in heart failure. I've posted the artcile down here 👇
P - In this double-blind trial, we randomly assigned 8442 patients with class II, III, or IV heart failure and an ejection fraction of 40% or less
I - 4187 patients to receive either LCZ696 (at a dose of 200 mg twice daily)
C- 4212 patients received Enalapril (at a dose of 10 mg twice daily), in addition to recommended therapy.
O- 'A total of 711 patients (17.0%) receiving LCZ696 and 835 patients (19.8%) receiving enalapril died, of these patients, 558 (13.3%) and 693 (16.5%), respectively, died from cardiovascular causes . As compared with enalapril, LCZ696 also reduced the risk of hospitalization for heart failure by 21% and decreased the symptoms and physical limitations of heart failure. The LCZ696 group had higher proportions of patients with hypotension and nonserious angioedema but lower proportions with renal impairment, hyperkalemia, and cough than the enalapril group'.
LCZ696 was superior to enalapril in reducing the risks of death and of hospitilization for heart failure
3. Diuretics reduce the preload
4. Use of Tab Ecosprin AV for prevention of stroke
This trial was randomized, double-blind and placebo-controlled.
P - Patients with ischaemic stroke but not complete paresis were included. Totally, 441 patients (220 aspirin, 221 placebo) completed the trial.
I - Tablets Aspirin 325 mg or placebo, water solvable, were administered orally once a day for five consecutive days.
Neurological assessments were carried out three times daily during the treatment period to detect progression of at least two points in the Scandinavian Stroke Supervision Scale.
Patient outcome was followed up at discharge and at 3 months
C - As regards patient outcome at discharge and after 3 months, aspirin treatment did not show any difference.
O - Aspirin treatment did not significantly reduce the frequency of stroke progression. Amongst aspirin‐treated patients, stroke progression occurred in 15.9% as compared with 16.7% in the placebo group, which is less frequent than expected. The relative risk was 0.95 in the treatment group.
This was a prospective, randomized, multicenter, double-blind, placebo controlled clinical trial of 4,731 patients with recent stroke or TIA and without known CAD who were randomized to receive either atorvastatin 80 mg daily or placebo
P- Patients who had had a stroke or TIA within one to six months before study entry, had LDL-c levels of 100 to 190 mg per dl and had no known CHD.
I- Atorvastatin 80 mg daily
C- Placebo
O- ‘During a median follow-up of 4.9 yrs, 265 patients (11.2 percent) receiving atorvastatin and 311 patients (13.1 percent) receiving placebo had a fatal or nonfatal stroke.
The atorvastatin group had 218 ischemic strokes and 55 hemorrhagic strokes, whereas the placebo group had 274 ischemic strokes and 33 hemorrhagic strokes.The overall mortality rate was similar, with 216 deaths in the atorvastatin group and 211 deaths in the placebo group, as were the rates of serious adverse events’
In patients with recent stroke or TIA and without known coronary heart disease, 80 mg of atorvastatin per day reduced the overall incidence of strokes and of cardiovascular events, despite a small increase in the incidence of hemorrhagic stroke.
The Non pharmacological interventions such as fluid restriction and salt restriction is to prevent fluid overload.
4) 31 yr old man with B/L pedal edema with scrotal and penile swelling since 2 months
a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
35 year old man
Complaining of
2 months history of bilateral pedal edema
Scrotal and penile swelling
History of palpitations few months back associated with dyspnea, sweating and dizziness
Occasional chest pain and nocturnal dry cough
Tingling in his lower limbs since 1 year
Difficulty in walking since a month
With a significant history of alcohol intake
This patient has Wet Beri Beri
The major manifestations of wet beriberi are tachycardia, cardiomegaly, high-output heart failure, and pedal edema, in addition to neuropathy.
Direct impairment of myocardial energy production has been proposed as a possible basis for the development of heart failure state seen in beriberi (because of loss of thiamine’s beneficial role in metabolic reactions). Decreased activity of pyruvate dehydrogenase due to thiamine deficiency results in build-up of pyruvate, which is then shunted towards anaerobic conversion into lactate. This accumulation of lactate causes a decrease in peripheral resistance, thereby increasing venous return to the heart (preload). This increase in preload coupled with myocardial dysfunction has been proposed to be a basis of congestive heart failure in thiamine deficiency. Wet beriberi mainly triggers right heart failure. The moderate pulmonary hypertension is common for wet beriberi patients.
Thiamine also helps in the conduction of nerve impulses, independent of its coenzyme functions. It is important for maintenance of nerve membrane stability and modulates membrane ion channels for efficient nerve conduction
Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes.
b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them?
Fluid and salt restriction to prevent overload
Diuretics to reduce preload
LEFT VENTRICULAR FUNCTION AFTER THIAMINE SUPPLEMENTATIONS IN PATIENTS WITH CHF
P - Thirty patients who were previously admitted with congestive heart failure and thiamine deficiency were selected and were put on double blind inpatient therapy
I - 15 patients received i.v. thiamine 200 mg/d
C - 15 patients received Placebo.
O - Thiamine status was determined by the erythrocyte thiamine-pyrophosphate effect (TPPE). LVEF was determined by echocardiography.
After i.v thiamine, TPPE decreased, LVEF increased as did diureses and sodium excretion. In the 27 patients completing the full 7-week intervention, LVEF rose by 22%.
Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy.
Thank you 😇
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