Negative pressure rooms

 Q: How frequently air should be changed in negative pressure rooms in ICU?

Answer:  6 to 12 air changes per hour 

Infected particles from respiratory secretions less than 5 microns can stay suspended in the air for a considerable period of time and may get inhaled by people in the surroundings. Airborne precautions are advised for infections like tuberculosis, measles, varicella, smallpox, and SARS viruses (including COVID-19). 

In ICUs airborne isolation is usually done in 'negative pressure rooms'. These rooms should have changed air for at least 6 to 12 times per hour. The door of the room needs to stay closed and caretakers should ideally be wearing N-95 masks. All healthcare workers should be tested for fitting their N-95 masks for a tight seal.

Said that, controversy does exist about negative pressure rooms' efficacy in protecting healthcare workers (see reference # 4).

#infectious-diseases 

Reference: 

1. Jensen PA, Lambert LA, Iademarco MF, et al. Guidelines for preventing the transmission of Mycobacterium tuberculosis in health-care settings, 2005. MMWR Recomm Rep 2005; 54:1.  

2. Wilder-Smith A, Low JG. Risk of respiratory infections in health care workers: lessons on infection control emerge from the SARS outbreak. Southeast Asian J Trop Med Public Health 2005; 36:481. 

3. Miller SL, Clements N, Elliott SA, Subhash SS, Eagan A, Radonovich LJ. Implementing a negative-pressure isolation ward for a surge in airborne infectious patients. Am J Infect Control. 2017 Jun 1;45(6):652-659.  

4. Braude D, Femling J. Dangerous Misperceptions About Negative-Pressure Rooms. Ann Emerg Med. 2020;76(5):690. doi:10.1016/j.annemergmed.2020.05.036

Highe PAOP

 Q: All of the following will have an elevated Pulmonary Artery Occlusion Pressure (PAOP) EXCEPT?

A) Left ventricular systolic heart failure 

B) Hypertrophic cardiomyopathy 

C) Cardiac tamponade 

D) Large pulmonary embolism 

E) Hypervolemia

Answer: D

Pulmonary artery occlusion pressure (PAOP), is also known as pulmonary capillary/artery wedge pressure (PCWP/PAWP). It estimates the left atrial pressure. It is ideally obtained with patient lying supine and at the end of expiration. The tip of the Pulmonary Artery Catheter (PAC) should be in zone 3 of the lung. Mean is obtained of the three previous readings to get the final reading. The balloon of PAC should be inflated while obtaining PAOP. The inflated balloon obstructs the blood flow through pulmonary artery and creates a static column of blood between the catheter tip and the left atrium. The pressure at both ends of the column gets equilibrates i.e., the pressure at the distal end of the catheter is equal to the pressure of the left atrium. Thus, PAOP is a reflection of left atrial pressure and a surrogate of the left ventricular end-diastolic pressure. 

Any condition that raises left ventricular end-diastolic pressure makes PAOP high. This includes left ventricular systolic or diastolic heart failure (choice A), mitral or aortic valve disease,  hypertrophic cardiomyopathy (choice B), cardiac tamponade (choice C), hypervolemia (choice E), and large right-to-left shunts. 

In contrast, conditions that deescalate or take away the pressure from the static column of blood between the catheter tip and the left atrium decreases the PAOP like hypovolemia, pulmonary veno-occlusive disease, or obstructive shock due to large pulmonary embolism (choice D).

We have put the original article on this concept from Drs. Swan and Ganz in the reference section below.

#hemodynamics

References:

1. Swan HJ, Ganz W, Forrester J, et al. Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med 1970; 283:447. 

2. Oliveira RK, Ferreira EV, Ramos RP, Messina CM, Kapins CE, Silva CM, Ota-Arakaki JS. Usefulness of pulmonary capillary wedge pressure as a correlate of left ventricular filling pressures in pulmonary arterial hypertension. J Heart Lung Transplant. 2014 Feb;33(2):157-62. doi: 10.1016/j.healun.2013.10.008. Epub 2013 Oct 11. Erratum in: J Heart Lung Transplant. 2014 Apr;33(4):459. de Oliveira, Rudolf K F [corrrected to Oliveira, Rudolf K F]. PMID: 24268673.

Diuretics and hyponatremia

 Q: Which of the diuretic is more prone to cause hyponatremia? (select one)

A) Thiazide

B) Loop

Answer: A

In thiazide diuretics, there is a direct effect of reduced sodium chloride reabsorption without water in the distal tubule, leading to hyponatremia.

Loop diuretics rarely cause hyponatremia. If hyponatremia occurs with loop diuretics, it pinpoints toward other underlying diseases such as congestive heart failure (CHF) or cirrhosis which are by default hyponatremic conditions. This protection of hyponatremia in loop diuretics is because the inhibition of sodium chloride transport in the loop of Henle impairs the generation of the countercurrent gradient. This limits the ability of Anti Diuretic Hormone (ADH) to promote water retention. 

#electrolytes

#nephrology

#pharmacology

References:

1. Szatalowicz VL, Miller PD, Lacher JW, et al. Comparative effect of diuretics on renal water excretion in hyponatraemic oedematous disorders. Clin Sci (Lond) 1982; 62:235. 

2. Filippone EJ, Ruzieh M, Foy A. Thiazide-Associated Hyponatremia: Clinical Manifestations and Pathophysiology. Am J Kidney Dis 2020; 75:256.

Sleep and vent weaning

 Q: Poor sleep quality in ICU leads to prolong weaning from mechanical ventilator? (select)

A) True

B) False

Answer: A

Sleep deprivation has clearly shown to deteriorate the normal respiratory process like hypoxic and hypercapnic chemosensitivity, tongue muscle's (genioglossus) performance, and inspiratory muscles' strength. Sleep studies in ICU have shown poor sleep quality to be associated with prolonged mechanical weaning time, and noninvasive ventilation failure.

#ventilators

References:

1. Thille AW, Reynaud F, Marie D, et al. Impact of sleep alterations on weaning duration in mechanically ventilated patients: a prospective study. Eur Respir J 2018; 51. 

2.  Chen HI, Tang YR. Sleep loss impairs inspiratory muscle endurance. Am Rev Respir Dis 1989; 140:907. 

3. Leiter JC, Knuth SL, Bartlett D Jr. The effect of sleep deprivation on activity of the genioglossus muscle. Am Rev Respir Dis 1985; 132:1242. 

4. Rault C, Sangaré A, Diaz V, et al. Impact of Sleep Deprivation on Respiratory Motor Output and Endurance. A Physiological Study. Am J Respir Crit Care Med 2020; 201:976. 

5. Roche Campo F, Drouot X, Thille AW, et al. Poor sleep quality is associated with late noninvasive ventilation failure in patients with acute hypercapnic respiratory failure. Crit Care Med 2010; 38:477.

Treatment failure in variceal bleed

 Q: 'Treatment Failure' in variceal bleed is defined by all of the following EXCEPT? (select one)

A) More than 100 mL of fresh blood in the nasogastric (NG) aspirate - 2 hours after endoscopic treatment

B) New hypovolemic shock 

C) Drop in hemoglobin of ≥3 g/dL (30 g/L) within 24 hours period

D) Bleeding ≥120 hours after the first hemorrhage, given hemostasis was initially achieved

Answer: D

The objective of this question is to highlight the specific terminologies used in variceal bleed. Variceal bleed and rebleed are two different entities. 

Time zero: – Time of admission. 

 Clinically significant bleeding:  - Transfusion requirement of at least two units of blood within 24 hours of time zero combined with a systolic blood pressure (SBP) less than 100 mmHg, a postural systolic change >20 mmHg, and/or a pulse rate >100 beats per minute at time zero. 

 Acute variceal bleeding: – The time interval from time zero to 120 hours. 

 Treatment failure: Any of the Choices A, B, and C above within 120 hours of time zero 

 Variceal rebleeding - (choice D)

#gastroenterology

Reference:

1. de Franchis R, Baveno V Faculty. Revising consensus in portal hypertension: report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension. J Hepatol 2010; 53:762. 

2. de Franchis R, Baveno VI Faculty. Expanding consensus in portal hypertension: Report of the Baveno VI Consensus Workshop: Stratifying risk and individualizing care for portal hypertension. J Hepatol 2015; 63:743. 

3. Tripathi D, Stanley AJ, Hayes PC, et al. U.K. guidelines on the management of variceal haemorrhage in cirrhotic patients. Gut 2015; 64:1680.

severe hyperthermia in SS

 Q: In severe hyperthermia associated with serotonin syndrome which is more effective? (select one) 

A) acetaminophen 

B) neuromuscular blockades 

 Answer: B

Antipyretic agents have no role in hyperthermia associated with serotonin syndrome as this hyperthermia is not hypothalamic regulated. The major reason for hyperthermia in serotonin syndrome is an increase in muscular activity.

This is one of the reasons that in extremely severe hyperthermia (read: only in extremely severe hyperthermia like above 41-degrees centigrade) intubation is preferred so a patient can be sedated well and muscle rigidity can be controlled with a long-acting nondepolarizing neuromuscular blocking agent such as vecuronium. 

Control of hyperthermia and muscle rigidity may prevent all further domino effects like seizures, coma, DIC, V. Tach, and metabolic acidosis.

#neurology

References:

1. Mills KC. Serotonin syndrome. A clinical update. Crit Care Clin 1997; 13:763. 

2. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005; 352:1112.

electrolyte in hepatic encephelopathy

 Q: Which electrolyte abnormality plays a role in the exacerbation of hepatic encephalopathy? (select one)

A) Hypokalemia

B) Hyponatremia

Answer: A

The presence of hypokalemia makes hepatic encephalopathy worse and should be corrected. Hypokalemia increases renal tubular production of ammonia. This ammonia enters back not only into the tubular lumen but also into the peritubular capillary. This process gets further exacerbated as these patients may also have concurrent metabolic alkalosis, which enhances ammonia's crossing of the blood-brain barrier. 

#hepatology

References:

1. Gabduzda GJ, Hall PW 3rd. Relation of potassium depletion to renal ammonium metabolism and hepatic coma. Medicine (Baltimore) 1966; 45:481. 

2. COOKE RE, SEGAR WE, CHEEK DB, et al. The extrarenal correction of alkalosis associated with potassium deficiency. J Clin Invest 1952; 31:798. 

3.  Artz SA, Paes IC, Faloon WW. Hypokalemia-induced hepatic coma in cirrhosis. Occurrence despite neomycin therapy. Gastroenterology 1966; 51:1046.

purpura fulminans

 Q: Fresh Frozen Plasma (FFP) is a reliable source of treatment in purpura fulminans (PF) due to meningococcemia?

A) True

B) False

Answer: B

The half-life of protein C in plasma is very short, and administration of FFP can't rely on for this purpose. Patients with meningococcemia may develop protein C deficiency which may lead to purpura fulminans. Ideally, these patients should receive 'protein C concentrate', which is given as a bolus followed by a q6 hours dose. The good guiding lab in such situations is the d-dimer level. Normalization or trend towards normalization of d-dimer is a sign that 'protein C concentrate' can be weaned or discontinued. 

FFP can be used as an alternative if 'protein C concentrate' is not available. It can be given every 6 hours or as a continued drip till clinical signs are resolved. But again, it can not be relied on to resolve the potentially life-threatening purpura fulminans. 

#hematology

#ID

References:

1. Smith OP, White B, Vaughan D, et al. Use of protein-C concentrate, heparin, and haemodiafiltration in meningococcus-induced purpura fulminans. Lancet 1997; 350:1590. 

2. Rintala E, Seppälä OP, Kotilainen P, et al. Protein C in the treatment of coagulopathy in meningococcal disease. Crit Care Med 1998; 26:965. 

3. Schellongowski P, Bauer E, Holzinger U, et al. Treatment of adult patients with sepsis-induced coagulopathy and purpura fulminans using a plasma-derived protein C concentrate (Ceprotin). Vox Sang 2006; 90:294.

Causes of death in ADPKD

Case: 58 years old male with a history of End-Stage Renal Disease (ESRD) due to Autosomal Dominant Polycystic Kidney Disease (ADPKD) was initially admitted for community-acquired pneumonia on a medical ward. Patient had a "code" and transferred to ICU. The most common cause of death in patients with ADPKD is? (select one)

A) cardiac disease 

B) infection/sepsis 

C) ruptured intracranial aneurysm 

D) hypertensive intracerebral hemorrhage 

E) renal cancer

Answer: A

In contrast to the conventional belief that most ADPKD patients die due to a neurologic event, the most common cause of death in these patients is cardiac. The majority of these patients develop hypertrophy and coronary disease. Only 12 percent of patients die due to hypertensive intracerebral hemorrhage (choice C) or ruptured intracranial aneurysm (choice D), a commonly associated finding in ADPKD. Infection (choice B) can be a cause too but renal cancer (choice E) has no relevance in ADPKD patients.

#nephrology

References:

1. Perrone RD, Ruthazer R, Terrin NC. Survival after end-stage renal disease in autosomal dominant polycystic kidney disease: contribution of extrarenal complications to mortality. Am J Kidney Dis 2001; 38:777. 

2. Fick GM, Johnson AM, Hammond WS, Gabow PA. Causes of death in autosomal dominant polycystic kidney disease. J Am Soc Nephrol 1995; 5:2048.

Lateral decub position and lungs reserve

 Q: What is the effect of lateral decubitus position on pulmonary ventilation perfusion? (select one) 

 A) perfusion increases in the dependent lung 

 B) perfusion increases in the non-dependent lung

Answer: A

In refractory hypoxemia changing of a patient's position is a frequent trick tried by clinicians at the bedside. It includes prone as well as lateral decubitus position. This may help or may make situation worse. Knowing one basic principle in conjunction with the extent of pathology in each lung may make it easier to decide on which side of lateral decubitus to choose (right vs left). 

In lateral decubitus position 

• Dependent lung: perfusion increases, ventilation decreases 
• Non-dependent lung: perfusion decreases ventilation increases 

 This ventilation perfusion mismatch occurs due to changed functional residual capacity and compliance.

#pulmonary

References: 

1. Larsson A, Malmkvist G, Werner O. Variations in lung volume and compliance during pulmonary surgery. Br J Anaesth 1987; 59:585. 

 2. Bhuyan U, Peters AM, Gordon I, Davies H, Helms P. Effects of posture on the distribution of pulmonary ventilation and perfusion in children and adults. Thorax. 1989;44(6):480-484. doi:10.1136/thx.44.6.480 

 3. Alcoforado L, Pessôa Filho LC, Brandão DC, Galvão AM, Reinaux CM, Andrade AD. Influence of change in lateral decubitus on pulmonary aerosol deposition. Rev Bras Fisioter. 2011 Aug-Sep;15(4):278-83. English, Portuguese. PMID: 21971723.

risk factor for mucormycosis

 Q; Pick one of the following as risk factor(s) for mucormycosis? 

 A) Iron overload 

 B) Deferoxamine 

 C) Iron and deferoxamine 

 D) Aluminum overload 

 E) Deferasirox 

 Answer: C 

 It is interesting that iron alone as well as in combination with its chelating agent Deferoxamine increases the risk for mucormycosis. Diabetic patients are extremely prone to develop mucormycosis. Clinically, it becomes significant to know as in diabetic ketoacidosis, free serum iron level goes up. One of the species for mucormycosis is Rhizopus. Increase iron uptake leads to its increased uptake by the fungus, it's growth, and tissue invasion. 

Traditionally deferoxamine is used as iron's chelating agent. The deferoxamine-iron chelate, known as feroxamine, is a siderophore for the species Rhizopus. This also enhances the iron uptake by the Rhizopus. 

Other iron-chelating agents, deferasirox and deferiprone, have not shown any such risks so far.   

#endocrinology

#ID

References:

1. Boelaert JR, de Locht M, Van Cutsem J, et al. Mucormycosis during deferoxamine therapy is a siderophore-mediated infection. In vitro and in vivo animal studies. J Clin Invest 1993; 91:1979. 

2. Maertens J, Demuynck H, Verbeken EK, et al. Mucormycosis in allogeneic bone marrow transplant recipients: report of five cases and review of the role of iron overload in the pathogenesis. Bone Marrow Transplant 1999; 24:307. 

3. Artis WM, Fountain JA, Delcher HK, Jones HE. A mechanism of susceptibility to mucormycosis in diabetic ketoacidosis: transferrin and iron availability. Diabetes 1982; 31:1109.

prevention of polymorphic VT with normal QT

 Q: Which of the following may prevent recurrent episodes in polymorphic Ventricular Tachycardia (VT) with a normal baseline QT interval?      

A) Beta-blocker (BB)

B) IV amiodarone

Answer:  B

The most common cause for polymorphic VT with a normal baseline QT interval is myocardial ischemia. If a patient is hemodynamically unstable then the first line of action is cardioversion, otherwise, BB and/or IV amiodarone is preferred. The need is to get rid of the underlying cause by emergent coronary angiography and revascularization. These patients frequently require transient mechanical support. IV amiodarone has the advantage of preventing recurrent episodes. Reflexly clinicians may order magnesium but it has no role in polymorphic VT with normal baseline QT.

#cardiology

Reference:

Sorajja D, Munger TM, Shen WK. Optimal antiarrhythmic drug therapy for electrical storm. J Biomed Res. 2015;29(1):20-34. doi:10.7555/JBR.29.20140147

Sepsis and glucose

Q: Severe sepsis results in? (select one)

A) hypoglycemia

B) hyperglycemia

Answer: A

Hypoglycemia is common in ICU. Factors commonly associated with hypoglycemia in ICU are underlying diabetes, kidney dysfunction, mechanical ventilation, high APACHE score, and severe sepsis or shock. One of the major reasons for hypoglycemia in ICU is the over-enthusiasm to achieve tight glucose control. 

As sepsis progresses, increased cytokines cause glucose utilization. Once utilization exceeds glucose production, hypoglycemia occurs. This is further complemented by cytokine-induced inhibition of gluconeogenesis. Another contributing factor in severe sepsis is ischemic liver (shock liver) leading to hypoglycemia.

#ID

#endocrinology

References: 

1. Krinsley JS, Grover A. Severe hypoglycemia in critically ill patients: risk factors and outcomes. Crit Care Med 2007; 35:2262. 

2. Maitra SR, Wojnar MM, Lang CH. Alterations in tissue glucose uptake during the hyperglycemic and hypoglycemic phases of sepsis. Shock 2000; 13:379. 

infectious rhombencephalitis

 Q: What is the most common cause of infectious rhombencephalitis?

Answer: Listeria meningitis 

Rhombencephalitis is also called brainstem encephalitis, and is clinically manifested as 

• ataxia
• cranial nerve palsies, and/or 
• nystagmus

Surprisingly, it occurs in healthy young adults. Diagnosis can be confirmed by aligning history, physical exam, blood cultures, lumbar puncture, and MRI. One of the cardinal features of history is the report of biphasic illness i.e., signs of brainstem dysfunction as described above first preceded by a prodromal flu-like syndrome. 

Ampicillin is the treatment of choice.

#infectious-diseaes

References:

1. Mylonakis E, Hohmann EL, Calderwood SB. Central nervous system infection with Listeria monocytogenes. 33 years' experience at a general hospital and review of 776 episodes from the literature. Medicine (Baltimore) 1998; 77:313. 

2. Charlier C, Perrodeau É, Leclercq A, et al. Clinical features and prognostic factors of listeriosis: the MONALISA national prospective cohort study. Lancet Infect Dis 2017; 17:510. 

3. Jubelt B, Mihai C, Li TM, Veerapaneni P. Rhombencephalitis / brainstem encephalitis. Curr Neurol Neurosci Rep. 2011 Dec;11(6):543-52. doi: 10.1007/s11910-011-0228-5. PMID: 21956758.

Treatments to avoid in rabies

 Q: 38 years old male is admitted to ICU with a history of exposure to bats and clinical symptoms pertinent to rabies. The patient required intubation due to progressive agitation and aerophobia. Which treatment modalities should be AVOIDED in patients with high suspicion of rabies?

Answer: In general there are no specific treatments for rabies. Most of the treatment is supportive though some antiviral, immunotherapies, cooling helmet, or nasal cooling has been described. The following treatments should be avoided in rabies as they can make symptoms worse or may harm the patient.

• Corticosteroids: May prevent the immune response required for viral clearance. 
• Minocycline: Described in literature but showed a harmful effect 
• Therapeutic coma: It requires paralytic which should be avoided as much as possible in rabies. 
•  Prophylaxis of cerebral vasospasm like nimodipine or Vitamin C: Vasospasm does not play a role in rabies

#infectious-diseases

References:

1. Jackson AC, Fu ZF. Pathogenesis. In: Rabies: Scientific Basis of the Disease and its Management, 3, Jackson AC (Ed), Elsevier Academic Press, Oxford 2013. p.299. 

2. Enright JB, Franti CE, Frye FL, Behymer DE. The effects of corticosteroids on rabies in mice. Can J Microbiol 1970; 16:667. 

3. Jackson AC, Scott CA, Owen J, et al. Therapy with minocycline aggravates experimental rabies in mice. J Virol 2007; 81:6248. 

4. Rossiter JP, Jackson AC. Pathology. In: Rabies: Scientific Basis of the Disease and its Management, 3, Jackson AC (Ed), Elsevier Academic Press, Oxford 2013. p.351.

ICP - earliest management

 Q: All of the following are the earliest bedside interventions in elevated Intracranial Pressure (ICP) secondary to intracranial hemorrhage (ICH) EXCEPT?

A) Elevation of  the head of the bed (HOB) to 30 degrees 

B) Sedation/analgesia for comfort 

C) Avoidance of endotracheal tube holder too tight

D) Normal saline for maintenance intravenous fluids (IVF) 

E) Glucocorticoids

Answer: E

Although sounds very simple but earliest interventions in high ICP play the highest modifying role in the trajectory of the outcome. Steroids have been suggested anecdotally as an intervention to reduce edema or inflammation due to high ICP in ICH but studies have shown no benefit. They are of benefit only in conditions where high ICP is due to an established inflammatory cause. Also, they can be judiciously used along with acetazolamide in patients who also develop severe papilledema. One of the less well-known dangers of steroids in high ICP is the rebound phenomenon during the tapering of the steroids. 

#neurosurgery

#neurology

#surgical-critical-care

#trauma

References:

1. Poungvarin N, Bhoopat W, Viriyavejakul A, et al. Effects of dexamethasone in primary supratentorial intracerebral hemorrhage. N Engl J Med 1987; 316:1229. 

2. Friedman DI, Jacobson DM. Idiopathic intracranial hypertension. J Neuroophthalmol. 2004 Jun. 24(2):138-45.

Hx in alcohol poisionings

 Q: What are the earliest classic symptoms of patients on presentation that may help to differentiate between methanol and ethylene glycol poisoning?

Answer: 

The classic of methanol poisoning includes complaining of any or all of 

• visual blurring
• central scotomata, and/or
• blindness

Patients with Ethylene Glycol patients are likely to complain of 

• flank pain
• hematuria, and/or
• oliguria

​The objective of the above question is to repeatedly highlight the importance of history taking, a rapidly disintigrating art in present day medicine.

#acid-base

#physical-exam

Reference:

Montjoy CA, Rahman A, Teba L. Ethylene glycol and methanol poisonings: case series and review. W V Med J. 2010 Sep-Oct;106(6):17-23. PMID: 21928557.

On Dig. toxicity

 Q: All of the following make chances of digoxin toxicity higher except?

A) hypokalemia 

B) hypomagnesemia 

C) hypercalcemia 

D) hypoxemia 

E) hyperthyroidism

Answer: E

Digoxin over the years is falling out of favor due to its narrow therapeutic index. Also, it can be affected by various electrolytes and underlying diseases particularly hypokalemia, hypomagnesemia, hypercalcemia, and hypothyroidism. In ICU, ventilated patients are prone to go into atrial fibrillation with the rapid ventricular rate (AF with RVR). Care should be taken while loading digoxin in such patients as hypoxemia increases the sensitivity of digoxin. Loading dose should be curtailed or guided by clinical response. 

Another issue is with digoxin's large volume of distribution. It gets widely distributed to skeletal and cardiac muscles as well as to lean tissues of the body. Patients with low muscle mass should have a limited loading dose. On the other hand, obese patients should not get a higher dose as dosing is based on body estimated lean weight and not on actual weight. Also, patients with renal insufficiency should get a conservative dose.

Answering the above MCQ - hypothyroidism reduces the volume of distribution and so the plasma clearance of digoxin and vice versa happens in hyperthyroidism (choice E).

#pharmacology

#cardiology

References:

1. MacLeod-Glover N, Mink M, Yarema M, Chuang R. Digoxin toxicity: Case for retiring its use in elderly patients?. Can Fam Physician. 2016;62(3):223-228. 

2. Should Digoxin Continue To Be Used for the Management of Atrial Fibrillation?. Can J Hosp Pharm. 2017;70(5):391-394. doi:10.4212/cjhp.v70i5.1701

normal Fibrinogen in sepsis

 Q: 77 years old female is admitted to ICU with severe urosepsis shock. Disseminated intravascular coagulation (DIC) panel was sent by an on-call resident.  Normal fibrinogen level in severe suspected sepsis is a good sign?

A) True

B) False

Answer: B

Hypofibrinogenemia is a cardinal feature of acute DIC. On the same token fibrinogen is also an acute phase reactant. So there are two paradox processes occurring in severe sepsis.

Production vs Consumption

In milder sepsis production of fibrinogen is usually lower than consumption. In patients with underlying severe sepsis (or cancer and inflammatory conditions), the production of fibrinogen is significantly higher. Normal plasma fibrinogen level is due to higher production than consumption in these patients and may deceive the bedside clinician.

#hematology

Reference:

Gruys E, Toussaint MJ, Niewold TA, Koopmans SJ. Acute phase reaction and acute phase proteins. J Zhejiang Univ Sci B. 2005;6(11):1045-1056. doi:10.1631/jzus.2005.B1045

SREC : HUS

 Q: Which of the following is the greater risk of clinical deterioration at the time of presentation in Shiga toxin-producing Escherichia coli (STEC) infections? 

A) hyponatremia 

B) hypernatremia

Answer: A

Hyponatremia at the time of hemolytic uremic syndrome (HUS) is found to be associated with bad outcomes. Aggressive intravenous fluid resuscitation is the mainstay of treatment with an isotonic solution. Oral resuscitation does not work in HUS due to two reasons. First, enteral electrolyte-containing solutions do not have enough sodium chloride to offer nephroprotection. Second, the severity of vomiting and abdominal pain hinders oral fluid resuscitation. Special attention should be paid as hyperkalemia can quickly develop in these patients due to brisk hemolysis and developing renal failure. 

Interestingly and less known fact about IV fluid resuscitation in STEC: HUS is that the adequacy is measured by hemodilution in the early phase which may require Hb level monitoring every 8 hours!

#infectious-diseases

References:

1. Alconcher LF, Coccia PA, Suarez ADC, et al. Hyponatremia: a new predictor of mortality in patients with Shiga toxin-producing Escherichia coli hemolytic uremic syndrome. Pediatr Nephrol 2018; 33:1791.

2. Ake JA, Jelacic S, Ciol MA, et al. Relative nephroprotection during Escherichia coli O157:H7 infections: association with intravenous volume expansion. Pediatrics 2005; 115:e673.

3. Grisaru S, Xie J, Samuel S, et al. Associations Between Hydration Status, Intravenous Fluid Administration, and Outcomes of Patients Infected With Shiga Toxin-Producing Escherichia coli: A Systematic Review and Meta-analysis. JAMA Pediatr 2017; 171:68.

uremic bleed

 Q: Which of the following is not recommended in a patient who is bleeding due to uremic dysfunction of platelets?

A) Transfusion of fresh platelets 

B)  Dialysis

C)  Desmopressin (DDAVP) 

D)  Estrogen 

E) Cryoprecipitate

Answer: A

In uremic platelet dysfunction transfusion of fresh platelets may not be very effective though clinicians have used this modality in desperate situations. Transfused platelets quickly acquire the uremic defect (choice A). 

One modality which is effective and in use for last 50 years is heparin free hemo or peritoneal dialysis, given stability of hemodynamic (choice B). 

Another preemptive strategy which is used in uremic patients undergoing invasive procedure is the administration of DDAVP (Choice C). 

Estrogen has been used effectively in dialysis patients who are prone to chronic gastrointestinal (GI) bleeding due to angiodysplasia or colonic polyps. In acute situations intravenous estrogen has also been found to be effective. Estrogen probably acts via decreased generation of Nitric Oxide (NO) (Choice D). 

Cryoprecipitate acts by the presence of substances in cryoprecipitate that enhances platelet aggregation, such as factor VIII:von Willebrand factor multimers or fibrinogen (Choice E).

It has also been argued that increasing the hemoglobin level to or above 10 g/dL reduces the bleeding time. 

#hematology

References:

1. Stewart JH, Castaldi PA. Uraemic bleeding: a reversible platelet defect corrected by dialysis. Q J Med 1967; 36:409. 

2. Zeigler ZR, Megaludis A, Fraley DS. Desmopressin (d-DAVP) effects on platelet rheology and von Willebrand factor activities in uremia. Am J Hematol 1992; 39:90. 

3. Kim JH, Baek CH, Min JY, et al. Desmopressin improves platelet function in uremic patients taking antiplatelet agents who require emergent invasive procedures. Ann Hematol 2015; 94:1457.

4. Livio M, Gotti E, Marchesi D, et al. Uraemic bleeding: role of anaemia and beneficial effect of red cell transfusions. Lancet 1982; 2:1013. 

5. Bronner MH, Pate MB, Cunningham JT, Marsh WH. Estrogen-progesterone therapy for bleeding gastrointestinal telangiectasias in chronic renal failure. An uncontrolled trial. Ann Intern Med 1986; 105:371. 

6. Viganò G, Gaspari F, Locatelli M, et al. Dose-effect and pharmacokinetics of estrogens given to correct bleeding time in uremia. Kidney Int 1988; 34:853. 

7. Janson PA, Jubelirer SJ, Weinstein MJ, Deykin D. Treatment of the bleeding tendency in uremia with cryoprecipitate. N Engl J Med 1980; 303:1318.

criteria for serotonin syndrome

 Q: Which of the following is more reliable for Serotonin Syndrome? (select one)

A) Hunter Criteria

B) Sternbach Criteria

Answer: A

Hunter Criteria is easy to perform at the bedside and has a specificity of 97 percent. The sensitivity is 84 percent. It is reliable even in milder or subacute situations. Beside history of serotonergic agent ingestion, it requires only one of the following

• Spontaneous clonus 
• Inducible clonus PLUS agitation or diaphoresis 
• Ocular clonus PLUS agitation or diaphoresis 
•  Tremor PLUS hyperreflexia 
•  Hypertonia PLUS temperature above 38ºC PLUS ocular clonus or inducible clonus

The Sternbach criteria is unspecific. Beside history of ingestion of serotonergic agent, it requires 3 out of the following 10 

1.  agitation
2. diaphoresis
3. ataxia
4. diarrhea
5. mental status change
6. hyperreflexia
7. myoclonus
8. tremor
9. shivering
10. hyperthermia

#neurology

References:

1. Dunkley EJ, Isbister GK, Sibbritt D, et al. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM 2003; 96:635.

2. Sternbach H. The serotonin syndrome. American Journal of Psychiatry. 1991;148:705-13.

Achalasia subtypes

 Q: According to Chicago Classification version 3.0 (CC-3), there are how many subtypes of achalasia?

A) One

B) Two

C) Three

D) Four

E) Five

Answer: C

Chicago Classification version 3.0 (CC-3) divides achalasia into three subtypes. Knowing these subtypes are important as management is different for each subtype. 

Type I is called classic achalasia. Clinically in this subtype, there is no significant change in esophageal pressurization due to swallowing. It has 100% failed peristalsis as indicated by a distal contractile integral (DCI) of less than 100 mmHg. 

In type Type II there is simultaneous pressurization which spans the entire esophagus due to swallowing. In this subtype, there is a 100% failed peristalsis and pan-esophageal pressurization in more than/equal to 20% of cases. 

Type III is called spastic achalasia. In this subtype, swallowing results in spasmatic and premature contraction. In this subtype, there is no normal peristalsis and premature (spastic) contractions is seen in more than/equal to 20% of swallows. 

 #surgical-critical-care 

 References:

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1. Kahrilas PJ, Bredenoord AJ, Fox M, et al. International High Resolution Manometry Working Group. The Chicago Classification of esophageal motility disorders, v3.0. Neurogastroenterol Motil. 2015;27(2):160–174.

2. Patel DA, Lappas BM, Vaezi MF. An Overview of Achalasia and Its Subtypes. Gastroenterol Hepatol (N Y). 2017;13(7):411-421.

HFNC and gas exchange

 Q: Higher the flow on High Flow Nasal Cannula (HFNC) higher the removal of PCO2? 

A) True

B) False

Answer: B

It is true that HFNC has come as a blessing for physicians and patients as it may mitigate the chances of invasive ventilation and re-intubations. It is now used with high frequency in ICUs. It has a lot of other advantages. It has a lot of other advantages. They are comfortable for patients with soft and pliable nasal prongs. With proper humidification and increased water content in mucous, it facilitates removal of secretion, decreases the work of breathing and so epithelial injury. Another significant advantage of HFNC is some degree of “PEEP/CPAP effect” which also helps in decreasing the work of breathing. To be precise, every increase of 10 L/minute of flow gives about 0.7 cm H2O of airway pressure with closed mouth and 0.35 cm of H2O with open mouth.

One disadvantage of HFNC is decreased CO2 removal. The inspiratory effort is inversely and linearly proportional to the level of the flow rate of oxygen. As the inspiratory effort goes down with higher levels of HFNC, it decreases CO2 removal.

#pulmonary-medicine

References:

1. Rittayamai N, Tscheikuna J, Rujiwit P. High-flow nasal cannula versus conventional oxygen therapy after endotracheal extubation: a randomized crossover physiologic study. Respir Care 2014; 59:485. 

2. Hasani A, Chapman TH, McCool D, et al. Domiciliary humidification improves lung mucociliary clearance in patients with bronchiectasis. Chron Respir Dis 2008; 5:81. 

3.  Parke R, McGuinness S, Eccleston M. Nasal high-flow therapy delivers low level positive airway pressure. Br J Anaesth 2009; 103:886. 

4. Mauri T, Alban L, Turrini C, et al. Optimum support by high-flow nasal cannula in acute hypoxemic respiratory failure: effects of increasing flow rates. Intensive Care Med 2017; 43:1453.

Bx of spleen

 Q: Biopsy of spleen can be safely performed at the bedside due to its easy access from Left Upper Quadrant (LUQ)  of abdomen?

A) True

B) False

Answer: B

The biopsy of spleen should be avoided as far as possible due to its high vascularity. If needed it should be done via endoscopic ultrasound (EUS) guided fine needle aspiration or CT guidance and with an experienced hand. It is recommended to observe the patient for a few hours even if the biopsy appears to be uneventful at the given moment. 

#surgical-critical-care

References:   

1. Mosquera-Klinger G, de la Serna Higuera C, Bazaga S, García-Alonso FJ, Sánchez Ocaña R, Antolín Melero B, et al. Endoscopic ultrasound-guided fine-needle aspiration for splenomegaly and focal splenic lesion: is it safe, effective and necessary?. Rev Esp Enferm Dig. 2020 May. 112 (5):355-359 

2. Katharine Hanlon, Matthew R. Wilson, David Kay, Bob Jackson, Mike Leach - Safety and diagnostic yield of splenic core biopsy; a methodical approach using combined Haematology/Radiology assessment in a tertiary referral centre. BJ Haem. Volume186, Issue2, July 2019, Pages 371-373, First published: 14 March 2019 https://doi.org/10.1111/bjh.15867

effusion in ESLD

 Q: 58 years old male with a history of cirrhosis is admitted to ICU with severe shortness of breath. Chest x-ray showed massive right sided effusion. Your next line of action is to insert right-sided chest tube?

A) Yes

B) No

Answer: B

The most common cause of portal hypertension is cirrhosis. Portal hypertension leads to many life-threatening complications including ascites, encephalopathy, variceal bleed, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome, hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy.

Hepatic hydrothorax is more of a mechanical pathology in comparison to pleural effusions due to cardiopulmonary disease. It is basically the movement of ascitic fluid into the pleural space through defects in the diaphragm, mostly visible on the right side of the chest x-ray. This is fundamentally important to understand as placement of a chest tube can be fatal in such a scenario, though repeated thoracenteses can be done to relieve the symptoms. The treatment is to target the underlying pathology of ascites with diuretics and sodium restriction. Transjugular intrahepatic portosystemic shunt (TIPS) can also be performed. The ultimate cure is usually liver transplantation.

#hepatology

References: 

1. Runyon BA, Greenblatt M, Ming RH. Hepatic hydrothorax is a relative contraindication to chest tube insertion. Am J Gastroenterol 1986; 81:566. 

2. Liu LU, Haddadin HA, Bodian CA, et al. Outcome analysis of cirrhotic patients undergoing chest tube placement. Chest 2004; 126:142. 

3. Orman ES, Lok AS. Outcomes of patients with chest tube insertion for hepatic hydrothorax. Hepatol Int 2009; 3:582. 

4. Ridha A, Al-Abboodi Y, Fasullo M. The Outcome of Thoracentesis versus Chest Tube Placement for Hepatic Hydrothorax in Patients with Cirrhosis: A Nationwide Analysis of the National Inpatient Sample. Gastroenterol Res Pract 2017; 2017:5872068.

Wound Vac

 Q: In the initial phase of Negative Pressure Wound Therapy (NPWT) - Wound Vac - the perfusion is increased? 

A) True

B) False

Answer: B

It is beyond the scope of this website to describe in detail the working of Wound-Vac. The negative pressure system of wound-vac generates a pressure gradient between the wound and suction canister. This negative pressure transports the fluid from wound bed and interstitial space and reduces wound edema. It also causes cell/tissue modulation. The pressure applied in wound-vac is 5-10 mmHg. Also, the foam in wound-vac system contracts and draws the edges of the wound together. 

Wound-Vac has also many indirect effects of wound healing. The major indirect effects are 

• Alterations in blood flow 
•  Diminished inflammatory response 
• Altered bacterial burden
• Changes in wound biochemistry

It was thought that negative pressure increases the blood flow/perfusion. In reality, this pressure leads to a paradoxical decrease in perfusion and causes local ischemia in the early phases. This ischemia stimulates the release of growth factors and vasoactive agents, leading to increase granulation and healing.

#surgical-critical-care

References:

1. Venturi ML, Attinger CE, Mesbahi AN, et al. Mechanisms and clinical applications of the vacuum-assisted closure (VAC) Device: a review. Am J Clin Dermatol 2005; 6:185. 

2. Kairinos N, Solomons M, Hudson DA. The paradox of negative pressure wound therapy--in vitro studies. J Plast Reconstr Aesthet Surg 2010; 63:174.

Asthma with eosinophilia

 Q: 48 years old female is admitted to ICU with severe exacerbation of asthma. Patient's blood workup showed significant eosinophilia with >1500 eosinophils/microL. What are few differential diagnoses?

Answer: Late presentation of exacerbation of asthma with significant eosinophilia should lead a clinician to think of other related diseases. Significant eosinophilia is defined as >15 percent or >1500 eosinophils/microL. Major catastrophic diseases should be ruled out besides allergic asthma such as 

• strongyloides 
• drug reactions 
• allergic bronchopulmonary aspergillosis 
• eosinophilic granulomatosis with polyangiitis (Churg Strauss), and 
•  hypereosinophilic syndrome

#pulmonary

References:

1. Bakakos A, Loukides S, Bakakos P. Severe Eosinophilic Asthma. J Clin Med. 2019;8(9):1375. Published 2019 Sep 2. doi:10.3390/jcm8091375 

2. Walford HH, Doherty TA. Diagnosis and management of eosinophilic asthma: a US perspective. J Asthma Allergy. 2014;7:53-65. Published 2014 Apr 11. doi:10.2147/JAA.S39119 

3. Bousquet J, Chanez P, Lacoste JY, Barnéon G, Ghavanian N, Enander I, Venge P, Ahlstedt S, Simony-Lafontaine J, Godard P, et al. Eosinophilic inflammation in asthma. N Engl J Med. 1990 Oct 11;323(15):1033-9. doi: 10.1056/NEJM199010113231505. PMID: 2215562.

4. Allen JN, Davis WB. Eosinophilic lung diseases. Am J Respir Crit Care Med 1994; 150:1423.

Vanco induced AKI

 Q: 58 years old female is admitted to ICU with vancomycin associated Acute Kidney Injury (AKI). Vancomycin associated AKI is likely to be reversible?

A) True

B) False

Answer: A

The basic pathology is the apoptosis induced by the accumulation of vancomycin in proximal tubular epithelial cells. There are many factors that can play a part including age, weight, pre-existing kidney disease, concurrent administration of other nephrotoxic drugs. In ICU the concurrent use of loop diuretics, aminoglycosides, amphotericin B, IV contrast, and vasopressors play an important role. In this regard more and more literature is coming out on AKI due to the coadministration of vancomycin and select beta-lactams like piperacillin-tazobactam and flucloxacillin. Both of these antibiotics are highly used in ICUs with vancomycin for broad-spectrum coverage. The average timeline in the development of AKI is about a week. 

Although there is no cutoff point to predict vancomycin-related AKI, one of the highest risks is the maintenance of Vanco trough level at 15 to 20 mg/L, a common practice in severe infections. 

Fortunately, two-third of patients recover on discontinuation of the drug and with other supportive treatment.

# nephrology

#pharmacology

#toxicology

References:

1. Sinha Ray A, Haikal A, Hammoud KA, Yu AS. Vancomycin and the Risk of AKI: A Systematic Review and Meta-Analysis. Clin J Am Soc Nephrol 2016; 11:2132. 

2. Avedissian SN, Pais GM, Liu J, et al. Piperacillin-Tazobactam Added to Vancomycin Increases Risk for Acute Kidney Injury: Fact or Fiction? Clin Infect Dis 2020; 71:426. 

3. Hidayat LK, Hsu DI, Quist R, et al. High-dose vancomycin therapy for methicillin-resistant Staphylococcus aureus infections: efficacy and toxicity. Arch Intern Med 2006; 166:2138. 

4. Carreno JJ, Kenney RM, Lomaestro B. Vancomycin-associated renal dysfunction: where are we now? Pharmacotherapy 2014; 34:1259. 

5. van Hal SJ, Paterson DL, Lodise TP. Systematic review and meta-analysis of vancomycin-induced nephrotoxicity associated with dosing schedules that maintain troughs between 15 and 20 milligrams per liter. Antimicrob Agents Chemother 2013; 57:734.

Age and SUDEP

Q: Older patients have a higher risk for Sudden unexpected death in epilepsy (SUDEP)?

A) True

B) False

Answer: B

Sudden unexpected death in epilepsy (SUDEP) has a specific definition: "The sudden, unexpected, witnessed or unwitnessed, nontraumatic, and non-drowning death in patients with epilepsy with or without evidence of a seizure, and excluding documented status epilepticus ≥30 minutes in duration, in which post mortem examination does not reveal a structural or toxicologic cause for death".

Interestingly, young patients between 18 and 40 years of age are at highest risk. It is rarely reported in older patients. Reason for this high prevalence in young patients is not known.

#neurology

References:

1. Nashef L, So EL, Ryvlin P, Tomson T. Unifying the definitions of sudden unexpected death in epilepsy. Epilepsia 2012; 53:227. 

2. Hughes JR. A review of sudden unexpected death in epilepsy: prediction of patients at risk. Epilepsy Behav 2009; 14:280. 

3. Harden C, Tomson T, Gloss D, et al. Practice guideline summary: Sudden unexpected death in epilepsy incidence rates and risk factors: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology 2017; 88:1674. 

4. Hitiris N, Suratman S, Kelly K, et al. Sudden unexpected death in epilepsy: a search for risk factors. Epilepsy Behav 2007; 10:138.