Conference Notes 4-10-2012   (Sorry for missing 4-3-2012 but I was in Atlanta for CORD)

BRAD KUTKA      CPC Case Presentation    

BEAU WILLISON/DENNIS RYAN   ORAL BOARDS

Case 1: Ascending Cholangitis :   Patient had Charcot’s Triad of Fever/Pain/Jaundice.   Reynold’s Pentad adds altered mental status and hypotension.  Treated with antibiotics and ERCP.

Case 2:Fitz Hugh Curtis.    Pt had PID Symptoms with RUQ pain.  Treated with iv Rocephin and Iv Doxy/ Azithromycin.

Case 3: Disseminated Zoster in a lymphoma patient on chemotherapy.   Treated with IV Acyclovir.  Panculture for neutropenia.   Cover with Cefipime as well.

ANDREA CARLSON    TOXIC MELTDOWNS

The hypothalamus triggers sweating in response to heat.  As you sweat, your serum osmolarity goes up.  At a certain point, high osmolarity will trigger the hypothalamus to decrease sweat losses to conserve fluids in body.

TCA’s can cause seizures, sweat gland dysfunction both factors in hyperthermia

Cocaine associated deaths are more frequent on hot days.

Hypothermia when sustained and severe causes denaturation of proteins and enzymes.

Hypothermia is the most important negative prognostic indicator for a drug overdose.

Serotonin Syndrome: Serotonergic medication AND  4 major or 3 major and 2 minor criteria.  Altered consciousness, mood change, coma, tremor, shivering, hyperreflexia, fever, rigidity, sweating, restlessness.  3 aspects of the syndrome: 1. Cognitive /behavioral  2. Autonomic changes  3. Neuromuscular findings.  Most common findings for these three arms are: confusion, fever, myoclonus. Common drugs: SSRI’s, amphetamines, Cocaine, tramadol, DXM, lithium, MAOI’s, methylene blue (multiple case reports), linezolid, metoclopramide, prochlorperazine.

Cyproheptadine is an old antihistamine.  Direct serotonin antagonist. Anecdotal evidence of improved survival in serotonin syndrome.  PO forms only available.

Neuroleptic Malignant Syndrome: due to dopamine deficit.  Slower in onset than Serotonin syndrome.  Altered mental status and rigidity precede hyperthermia and autonomic instability.   Bradykinesia and “lead pipe rigidity”  are key neuro findings.

For both SS and NMS you gotta cool the patient.   Control seizures,  give benzos, give Dantrolene (dantrolene is a skeletal muscle relaxant and can make a pt weak but not paralyzed).  Bromocriptine for NMS, Cyproheptadine for SS.   Use other cooling measures like fans and misters.  No reports yet of using cool guard to bring down pt’s temp.   

TONY GRIPPO   TRAUMATIC BRAIN DEATH

Uniform Death Act  1981 makes brain death equivalent to cardiovascular death.

Prerequisites: Know cause of coma, normothermia, no drug intoxication/poisoning.  ETOH < 80.  No treatable metabolic causes.   BP>100systolic.

Exam: Coma; completely unresponsive to noxious stimuli.     Absent Brain Reflexes; no papillary light reflex/no corneal reflex/no ocular movement to cold calorics or doll’s eyes/response to painful stimuli above the neck/no jaw jerk/no gag or cough with suctioning.      Apnea;Vent disconnected, o2 given via tracheal canula.  If after  10 minutes pCo2 of 60 or greater and no breath that is positive for brain death.  Need two tests to be definitive.   If apnea test is inconclusive you can do nuclear medicine testing or cerebral angiography.   Nuclear medicine scan shows “empty light bulb” and “hot nose” findings when positive for brain death.

Lazarus reflex: There are some spinal reflexes even though the patient is brain dead.  Neck flexion can cause upper extremity flexion even though brain death is present.   Cremasteric reflex is preserved. There are other toe and finger reflexes that persist after brain death as well.

You have to wait 72 hours after therapeutic hypothermia (some say 6 days) before you can start considering for brain death.

Brain dead patients are the source of 50% of renal transplants and majority of extra renal organ transplants.   

Supporting the brain dead patient to maintain organ perfusion  should include volume infusion, pressor management,  and  hormone replacement therapy.   Dopamine first  and  then vasopression if needed are  the recommended pressors.  Amiodarone is the recommended antiarrythmic.   Hormonal resuscitation includes T3, Vasopressin, Methylprenisolone, and Insulin.

MARK HINTON   M&M

Pt on Coumadin falls and hits head. Subtle mental status changes.  Initial CT was neg.  INR was prolonged to 5 range.  Pt came back 1-2 days later for increased mental status changes and ataxia and renal insufficiency.  Family notes on second visit that pt has  been having multiple falls.  Pt found to be digoxin toxic. 

Digoxin toxicity:

Sources of error: minimizing problems by patient.   Recall biases,  Attending/Resident discrepencies.  Anchor bias,  premature closure.

William Withering discovered digoxin in 1785.  Treated dropsy.

Foxglove, oleander, and lily of the valley are botanical sources of digoxin.  You can also get digoxin toxic from licking the skin of toads (also hallucigenic).

Digoxin is mostly eliminated renally.

Ekg changes with therapeutic digoxin level, lateral/inferior  st depression with downsloping st segment and inverted t wave.   

First symptoms of overdose are somnolence, dizziness, and confusion.

Causes of toxicity: overdose, renal insufficiency, and drug interations (amiodarone, verapamil, vytorin, other statins, macrolides).

EKG changes in toxicity: pvc’s, any svt with av block, pat with block is pathognomonic, bidirectional V-tach, sinus bradycardia, slow afib,  regularized afib,

Severity of hyperkalemia correlates with mortality.

Xanthopsia: yellow vision.   Did Van Gogh suffer from digoxin toxicity?  He painted his doctor sitting with a foxglove plant nearby.

Treat hyperkalemia with  standard treatement insulin/dextrose, bicarb, kayexelate.  Calcium now thought to be ok for hyperkalemia.    Digibind treats the digoxin overdose and the hyperkalemia.   Digibind works in about 30-60 minutes.   Digibind is safe in kids down to 12 weeks old.