TTP: quick review

27 Oct

TTP is thrombotic thrombocytopenic purpura, characterized by a pentad (FATRN)

  • Fever,
  • Anemia (microangiopathic hemolytic),
  • Thrombocytopenia,
  • Renal dysfunction,
  • Neurologic dysfunction (that may be transient)

All of these are present only 1/3 of the time.

 

- TTP occurs usually in adults and rarely in children, while HUS is more common from age 6 mos to 5 years.

- TTP is a hematologic emergency with 100% mortality if untreated, and 10-20% if treated- bad stuff.

 

- If TTP is suspected, steroids should be started, give FFP, and consult hematology for plasma exchange therapy.

 

- Why FFP?

As in treatment of hereditary angioedema which lacks C1 esterase, in TTP the protease ADAMTS13 (aka vWF-cleaving protease) is qualitatively or quantitatively absent, but this is found in FFP.

 

- Avoid platelet transfusion unless there is bleeding that will kill the patient before TTP does, as platelet replacement may exacerbate the thrombus formation.

 

- All of the pentad are cause by the effects of large, uncleaved vWF monomers clumping with platelets, causing unstable thrombi that transiently cause vessel occlusions, leading to renal and neurologic dysfunction, the shearing of RBCs in the small vessels, and low platelets.

 

- So what causes TTP anyway?

It is associated with HIV, flu vaccination, acute pancreatitis, and often medication use including Plavix, flouroquinolones, resperdol, valacyclovir, and infliximab, among others.

 

References: Koyfman A. Thrombotic Thrombocytopenic Purpura.[Review] Pediatric Emergency Care. 27(11):1085-1088, November 2011.; uptodate.com; picture

visual aid: biceps tendon rupture

24 Oct

Good visual aid from the September EP Monthly mag.  The article has some deeper info, but in a pinch, remember to look for this:

a.k.a. the Popeye deformity.

There you go.

 

References: epmonthly article; popeye

Snake Bite (part 2): management pearls

21 Oct

ED Management:anklebite

  • Limb Elevation
    • Avoid pressure immobilization (tourniquets)
  • Wound Demarcation
    • Assess every 15-30 min
  • Pain Control
    • IV Opioids
  • Toxicology C/S
  • Tetanus ppx

 

Note:  No indication for FFP and platelets.  Both are inactivated by Crotalinae venom. 

 

Antivenom (Crofab):

Tx for significant Crotalinae envenomation in the U.S.anklebite3

 

  • Dosing
    • Mix 4-6 vials of crotalinae Fab antivenom (Crofab) in 250 mL NS.
    • Infuse IV over 1 hr.
    • Pediatric antivenom dose = Adult dose

 

Anaphylaxis to Antivenom:

  • Epinephrine3 – 0.5 mg IM (1 mg/mL preparation):
    • Repeat q5-15min PRN.
  • Steroids
    • Methylprednisolone 125 mg IV.
  • Antihistamine
    • 25 to 50 mg IV
  • Oxygen
    • 8-10 L/min via facemask

 

 

ED Disposition:

  • Treated with antivenom
    • Hospital admission for further observation and supportive care.
  • No antivenom administration
    • Discharge home if:
      • No clinical signs of toxicity
      • 8-10 hours c/ normal coagulation panel

 

Submitted by Christina Brown.

 

References: 

  • Walter FG, Chase PB, Fernandez MC, McNally J. Venomous snakes. In: Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose, 4th, Shannon MW, Borron SW, Burns MJ (Eds), Saunders, Philadelphia 2007. p.399.
  • Lavonas EJ, Ruha AM, Banner W, et al. Unified treatment algorithm for the management of crotaline snakebite in the United States: results of an evidence-informed consensus workshop. BMC Emerg Med 2011; 11:2.
  • American College of Medical Toxicology, American Academy of Clinical Toxicology, American Association of Poison Control Centers, et al. Pressure immobilization after North American Crotalinae snake envenomation. J Med Toxicol 2011; 7:322.
  • American College of Medical Toxicology, American Academy of Clinical Toxicology, American Association of Poison Control Centers, et al. Pressure immobilization after North American Crotalinae snake envenomation. Clin Toxicol (Phila) 2011; 49:881.
  • Yip L. Rational use of crotalidae polyvalent immune Fab (ovine) in the management of crotaline bite. Ann Emerg Med 2002; 39:648.

Snake Bite (part 1): recognition

20 Oct

Epidemiology:anklebite

Most common venomous snakes in the U.S.

  • Rattlesnakes, Water moccasins (cottonmouths), Copperheads
  • Venomous = Triangular shaped head, elliptical pupils

 

Local Toxicity

  • Swelling, pain, ecchymosis, tissue necrosis and blistering
    • Proteolytic  

 

Systemic Toxicity

  • Coagulopathy
    • Thrombocytopenia
    • Thrombin-like glycoproteins in venom

 

  • Rhabdomyolysis
    • Enzymatic tissue damage adjacent to the bite.
    • Renal Failure

 

  • Compartment Syndrome
    • Subcutaneous edema

 

  • Other:
    • Hypotension, respiratory distress, oral paresthesia’s
    • Abdominal pain, vomiting and dizziness

 

Primarycopperhead

  • Airway, Breathing, Circulation
    • Angioedema, Bleeding, Hypotension

 

Secondary

  • Wound Site:
    • Swelling, pain, ecchymosis, tissue necrosis and blistering
  • Systemic Signs:
    • Oral paresthesias, refractory vomiting, abdominal pain and neurotoxicity

 

Lab Studies:

  • Coagulopathy
    • PT/PTT, INR
    • Fibrinogen
    • D-dimer
  • BMP, CBC
  • CK
  • EKG

Signs of envenomation: 

  • Prolonged PT
  • Decreased Fibrinogen or Platelets

 

Submitted by Christina Brown.

 

References: 

  • Walter FG, Chase PB, Fernandez MC, McNally J. Venomous snakes. In: Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose, 4th, Shannon MW, Borron SW, Burns MJ (Eds), Saunders, Philadelphia 2007. p.399.
  • Lavonas EJ, Ruha AM, Banner W, et al. Unified treatment algorithm for the management of crotaline snakebite in the United States: results of an evidence-informed consensus workshop. BMC Emerg Med 2011; 11:2.
  • American College of Medical Toxicology, American Academy of Clinical Toxicology, American Association of Poison Control Centers, et al. Pressure immobilization after North American Crotalinae snake envenomation. J Med Toxicol 2011; 7:322.
  • American College of Medical Toxicology, American Academy of Clinical Toxicology, American Association of Poison Control Centers, et al. Pressure immobilization after North American Crotalinae snake envenomation. Clin Toxicol (Phila) 2011; 49:881.
  • Yip L. Rational use of crotalidae polyvalent immune Fab (ovine) in the management of crotaline bite. Ann Emerg Med 2002; 39:648.

opiod converter

16 Oct

came across this handy calculator at GlobalRPH.com.

everyone metabolizes a bit differently, of course, but if you’re curious about ballpark equivalences among the different opiates, check out the link to the calculator.

convert

 

References: globalRPH

 

aortoenteric fistula: fear it

13 Oct

QUICK PEARLS:

Aortoenteric fistula: a communication between the aorta and the GI tract

consider in anyone with a GI bleed and a history of aortic surgery.

Can involve any part of the bowel but 75% involve the third part of the duodenum.

Mean time to presentation from surgical date is 32 months, but can run the gamut.

 

Can be primary (from AAA, but this is rare), but often related to aortic graft

 

Herald Bleeds

  • often have self-limited “herald bleeds”, can be intermittent
  • Stops from vasospasm or thrombus formation
  • Followed by massive GI bleed over the next month; 30% of these are within next 6 hours

 

DIAGNOSIS:

  • Conventional CT
  • CTA (most sensitive with “detection rate” of 61%)
  • EGD (25-62.5% or primary fistulas are identified)
  • Laparotomy

 

TREATMENT OPTIONS:

  • Endovascular stent for those than cannot tolerate surgery
  • Graft resection, repair of duodenal wall, and new bypass (mortality rate: 30-40%)
  • Gentle resuscitation: SBP goal 60-100
  • Survival rates with treatment: 30-70%

 

References:  MacDougall, L et al. Aorto-enteric fistulas: a cause of gastrointestinal bleeding not to be missed.  BJMP. 2010; 3(2): 317.   Ranasinghe, W et al. Primary aortoenteric fistulae: the challenges in diagnosis and review of treatment. Ann Vasc Surg. 2011; 25(3): 386; picture

intractable hiccups?

9 Oct

SOME INTERESTING DEFINITIONS:

involuntary, intermittent, spasmodic contraction of the diaphragm and intercostal muscles.

Muscle contraction results in a sudden inspiration and ends with abrupt closure of the glottis, thereby generating the characteristic ‘hic’ sound.

often occur with a frequency of 4 to 60 per minute

The medical term for hiccups (also referred to as ‘hiccoughs’) is singultus, derived from the Latin singult, which means ‘a gasp’ or ‘a sob.’

 

SOME PHYSIOLOGY:

exact mechanism provoking hiccups remains unknown.

involve unilateral contraction of the left hemidiaphragm in ~80%

pathways involve phrenic and vagus nerves

 

COMMON CAUSES:

  • gastric distention from overeating,
  • carbonated beverages,
  • swallowing with chewing gum or smoking
  • gastric insufflation during endoscopy
  • sudden changes in ambient or gastrointestinal temperature
  • excessive alcohol ingestion.
  • Sudden excitement or other emotional stress

LESS COMMON CAUSES:

the list of less common, but potential causes is broad, e.g.

  • CNS disorders
  • vagus or phrenic nerve irritation
  • GI disorders
  • thoracic disorders
  • cardiac
  • tox
  • post-op
  • psychogenic

Message: if they have other odd or associated symptoms, consider chasing them to a broader differential.

 

POSSIBLE TREATMENTS:

Non-medication (a fun list, with mostly little downside):

Breath holding
Valsalva maneuver
Breathing into bag
Ice water gargles
Swallowing granulated sugar, hard bread, or peanut butter
Drinking from opposite side of glass
Catheter or cotton swab stimulation of nasooropharynx
Forceable traction on the tongue
Biting on a lemon
Fright
Noxious odors (inhaling ammonia)
Pressing on the eyeballs
Pulling knees to chest or leaning forward to compress the chest

 

Medication options:

first suggestions involve chlorpromazine, reglan, or baclofen.

cyclobenzaprine, haldol are also among the more readily ED available meds on the list.  often these meds are not expected to work immediately.

 

References: uptodate.com; picture

 

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