Learning Critical Care Medicine

“When using a sphygmomanometer, we pauperize our senses and weaken clinical acuity.”           ­- British Medical Journal, some 100 years ago, on forgetting art of arterial pulse analysis. Qualitative arterial pulse wave analysis has been exploited, for millennia to diagnose various diseases, by Indians, Chinese, Greeks and Roman physicians. Gallen described 27 type of pulses, in ‘on Prognosis from the Pulses’ written before 210 AD, and Wang Shu-he gave description of 24 types of pulses, in Mai Jung, in 220 AD. Traditional Indian teaching had largely been oral, from master to student, hence little documentation is available. Quantitative arterial pulse wave analysis was first attempted by, Leonhard Euler in eighteen century, when he applied the principle of conservation of mass and energy, to a tubular model of cardiovascular system. Frederick Akbar Mohamed established the foundation of pulse wave analysis, in a short medical lifetime, from 1872 to 1884. He described th

“It is astonishing that no one has arrived, at the following obvious method, by which the amount of blood ejected by the ventricle of the heart with each systole, may be determined directly……”  -Adolf Fick, July 9, 1870, On Fick Principle, In proceedings of Würzburg Physikalische Medizinische Gesellschaft. Primary determinant of organ perfusion is blood pressure (mean arterial pressure- MAP). Blood pressure itself is product of cardiac output (CO) and  systemic vascular resistance (SVR).                                    MAP= CO × SVR This physiological equation can have variety of permutation and combination in different pathological states. Low MAP could be the result of,          low CO and high SVR (hypovolemic and cardiogenic shock)         high CO and low SVR (vasodialatory shock- septic, anaphylactic, neurogenic) Normal MAP could be the result of         low CO and high SVR ( high dose vasopressors in the setting of hypovolemia or cardiac dysf

"Na tha kuchh to Khuda tha,kuchh na hota to Khuda hota, duboya mujhko hone ne, na hota main to kya hota"                                                        - Mirza Ghalib Paroxysmal sympathetic hyperactivity (PSH) is a syndrome, recognized in a subgroup of severe acquired brain injury patients, of rapid onset, paroxysmal episodes of agitation and dystonia, in association with autonomic symptoms like tachycardia, hyperventilation, fever, diaphoresis and pupillary dilation. The first case of PSH was reported by Penfield in 1929, as diencephalic autonomic epilepsy. He hypothesized that these episodes are caused by epileptiform discharges in thalamic nuclei, irritated by increased intracranial pressure, a theory which was later refuted. It has been described in literature by different names like dysautonomia, central autonomic dysfunction, paroxysmal sympathetic storms, midbrain dysregulatory syndrome and paroxysmal autonomic instability with dystonia (PAID). While PSH

"No bubble is so iridescent or floats longer than  that blown by the successful teacher"                                                       -William Osler Clostridium difficile, a spore-forming gram-positive anaerobic bacillus, was initially detected in the fecal flora of healthy newborns in 1935. Clostridium difficile was thought to be nonpathogenic until 1978, when Bartlett et al identified C. difficile as the source of cytotoxin in the stools of patients with pseudomembranous colitis, a disorder frequently associ- ated with antimicrobial use. Clostridium difficile infection (CDI) range from asymptomatic carrier, to mild diarrhea, to fulminant pseudomembranous colitis. C. difficile associated diarrhea (CDAD) is the most common cause of infectious diarrhea in hospital setting. It accounts for 20-30% cases of antibiotic associated diarrhea. It is associated with passage of mucus or occult blood in stool, but melena or hematochezia are rare. Fever, cramping, abdominal d

"one can mimic the result, but can not mimic the creativity" Sepsis is the clinical syndrome that results from a dysregulated inflammatory response to an infection, often leading to organ dysfunction. It is still associated with high mortality and financial burden. Sepsis is one of the challenge, that keeps on intriguing critical care physician time and again. Several diseases closely masquerade sepsis, due to similar pathophysiology of immune modulation.  Sometimes it becomes challenging to differentiate sepsis from these mimics as critically ill patients have multiple confounding factors from hospital acquired infections to drug interactions and toxicity. ●LINEZOLID INDUCED LACTIC ACIDOSIS : Linezolid is the precious arsenal for VRSA (vancomycin resistant staph. aureus), VRE (vancomycin resistant enterococcus) and MDR tuberculosis. • Presentation of linezolid induced lactic acidosis is characterized by nausea, pain abdomen, altered mental state, hypo

“The only man who behaves sensibly is my tailor; he takes my measurements anew, every time he sees me, while all the rest go on with their old measurements and expect me to fit them”.                                                                                                 -George Bernard Shaw Cranium is a fixed space, containing brain tissue, CSF, and blood. In an adult, total inracranial volume is 1475 ml. This consists of 1300 ml brain parenchyma, 65 ml if CSF and 110 ml of blood. Intracranial pressure (ICP) is, pressure exerted by the cranial content, on dura mater. Pressure is built by, arterial flux and depends on the volume, and therefore partial pressure, of each component of skull's content.                  ICP = P brain + P blood + P csf If one component pressure of ICP increases (for example, if brain oedema develops and 'P brain' increases), other component pressures should decrease, to keep ICP constant, as per Monro Kellie doctrine. Compensatory m

"It ain't what people don't know, that hurt them, It's what they know, that ain't so".                                                    -Josh Billings Evidence based medicine is quite frequently, not translated into, clinical practice. This may be due to the fact that, clinical practice is often guided by personal preference, and subjective sense of security, provided by conventional medical wisdom. Use of prophylactic antiepileptic drugs (AED) in neurocritical care, is not an exception to this phenomenon. Evidence suggests that, only in traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (aSAH), there may be some benefit of, short course prophylactic AED, by preventing early onset seizures. ●TRAUMATIC BRAIN INJURY (TBI): Posttraumatic seizures (PTS) in TBI patients are classified as early posttraumatic seizure (occurring within first 7 days of injury) and late posttraumatic seizure (occurring after 7 days of injury). Incidence of earl

"I'll be your mess, you be mine, That was the deal that we had signed, I bought a hazmat suit to clean up your waste, Gas masks, gloves, to keep us safe, But now I'm alone in an empty room, Staring down at immaculate doom."      -Where she went; Gayle Forman In our material world,  Effect can't be divorced from side effect. And the end result is, not always, the calculated balance beween these two, at least in sociopolitical world. Intervention in clinical medicine also embraces this truth, but awareness, measures of prevention and effective treatment can decrease the severity of side effect. ●Immune Restoration Disease (IRD) or Immune Reconstitution Inflammatory Syndrome  (IRIS): Restoration of immune response against living or dead opportunistic pathogen causes immunopathological lesion in tissues infected by that pathogen. First described in HIV infected patients, where commencing antiretroviral therapy (ART) may cause paradoxical worsening of opportu

"Primum non nocere" First, do no harm. One of the rule of practicing good medicine, is to know precisely, what not to do, to avoid catastrophe,  to the patient as well as the physician. ●INSULIN INFUSION BEFORE CORRECTING POTASSIUM, in hyperglycemic states: Adult patients presenting with Diabetic Ketoacidosis or Hyperosmotic hyperglycemic state, usually have total body potassium deficit of about 300-600 mEq/L. It is the result of osmotic diuresis and secondary hyperaldosteronism. Despite this serum potassium is usually normal or in one third of cases, may be elevated on admission, due primarily to insulin deficiency and hyperosmolality,  both of them drive potassium out of cells. Insulin infusion will reverse this movement and cause dramatic fall in serum potassium concentration. Which can lead to life threatening cardiovascular and neuromuscular complications. Therefore insulin infusion should not be started if serum Pottasium is less than 3.3 mEq/L. Potassium must be

"Dil e nada tujhe hua kya hai, Akhir is dard ki dawa kya hai"                 - Mirza Ghalib 76 Y F admitted with severe chest pain, which started 4 hours back after hearing news of her sister's death. She  had no history of coronary artery disease. Evaluation suggested BP 90/50 and HR of 100. JVP was not elevated, no murmur heard, chest auscultation revealed vesicular sounds, and extremities were warm. EKG showed ST elevation with T inversion in anterior leads. Cardiac enzymes were mildly raised. Echo showed left ventricle apical akinesia  with hypercontractile basal wall. Abnormal dilatation of LV was seen during systole. Emergency coronary angiography revealed normal coronaries. TAKOTSUBO CARDIOMYOPATHY : CLINICAL PRESENTATION  is similar to acute myocardial infarction with substernal chest pain and dyspnoea. EKG mimics ST elevation or T wave inversion, most commonly in anterior leads. Cardiac enzymes are mildly elevated. ECHOCARDIOCARDIOGRAPHY shows depresse