Tag Archives: tox

What is Palcohol?

17 Jul

some tidbits for the near-the-horizon coming of Powdered ALCOHOL (Palcohol), via this month’s EM News:

 

concentrated powdered alcohol

>= 55% alcohol by weight, 10% by volume

palcohol

the idea:

mix with warm water, imbibe

the concerns:

hidden ingestion (e.g. slipping it into drinks, spiking food)

non-PO routes (e.g. snorting, IV)

 

deterrents (hopefully)

volume — packet says 200ml with water added, so would take a lot powder to spike/snort/shoot 1 shot of liquor’s worth

pain — snorting or IV injection seems caustic and painful

 

There you go.  Be on the lookout.

 

References: EM News article + picture; SA article

 

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Isopropyl Alcohol (part 2) – Management

18 May

(check out the previous post for some initial isopropyl alcohol tidbits)

WHAT TO ORDER, WHAT TO LOOK FOR:

Tests to obtain — The following tests should be obtained in all poisoned patients:

  • POC glucose
  • Acetaminophen and salicylate levels, to rule out these common co-ingestions
  • Electrocardiogram (ECG), to rule out conduction system poisoning by drugs that affect the QRS or QTc intervals
  • Pregnancy test in women of childbearing age
  • Serum isopropyl alcohol and acetone levels (or serum osmolality, if direct serum drug levels are unavailable). 
  • Basic electrolytes, with calculation of anion gap
  • BUN and creatinine
  • Serum and urine ketones
  • Arterial or venous blood gas

 

Elevated Osmolar Gap. The absence of a high anion gap metabolic acidosis four to six hours post-ingestion enables the clinician to distinguish from other alcohols.

 

Serum concentrations of at least 100 mg/dL (17 mmol/L) are necessary to cause a decreased level of consciousness. 

Both isopropyl alcohol and acetone will raise the osmolal gap.

The plasma osmolal gap cannot distinguish among isopropyl alcohol, methanol, and ethylene glycol poisoning, and so cannot be used to exclude ingestion of these more toxic alcohols.

 Calculated Sosm   =   (2 x serum [Na])  +  [glucose]/18  + [BUN]/2.8

 

MANAGEMENT – ABC’s, then…

Decontamination — There is no role for gastrointestinal (GI) decontamination in most cases of isolated isopropyl alcohol intoxication. Its rapid absorption after oral ingestion and its low toxicity make such interventions unnecessary.

 

Alcohol dehydrogenase (ADH) inhibition — Since acetone (the primary metabolite) is less toxic than isopropyl alcohol (the parent alcohol), there is no indication for ADH inhibition with fomepizole or ethanol following isopropyl alcohol exposure

 

Disposition – Symptoms from isopropyl alcohol manifest quickly. Therefore, patients with unintentional ingestions can be discharged after two hours if they remain asymptomatic and isopropyl alcohol is known to be the only substance involved.

 

Submitted by Christina Brown.

 

References: uptodate.com; Trullas JC, Aguilo S, Castro P, Nogue S. Life-threatening isopropyl alcohol intoxication: is hemodialysis really necessary? Vet Hum Toxicol 2004; 46:282.; Stremski E, Hennes H. Accidental isopropanol ingestion in children. Pediatr Emerg Care 2000; 16:238.;  Bekka R, Borron SW, Astier A, et al. Treatment of methanol and isopropanol poisoning with intravenous fomepizole. J Toxicol Clin Toxicol 2001; 39:59.;  Su M, Hoffman RS, Nelson LS. Error in an emergency medicine textbook: isopropyl alcohol toxicity. Acad Emerg Med 2002; 9:175.; picture

Isopropyl Alcohol (part 1) – Recognition

15 May

ISOPROPYL ALCOHOL – Central nervous system (CNS) inebriant and depressant.  Toxicity and treatment resemble that of ethanol.

 

EPIDEMIOLOGY – Fatality from isolated isopropyl alcohol toxicity is rare, but can result from injury due to inebriant effects, untreated coma with airway compromise, or rarely, cardiovascular depression and shock following massive ingestion. 

 

PHARMACOLOGY AND TOXICOLOGY — a CNS depressant whose toxicity closely resembles that of ethanol, with which it shares strong structural similarity.  

In untreated animals, the median lethal dose lies between 4 and 8 g/kg.

Isopropyl alcohol does NOT cause an elevated anion gap acidosis, unlike the toxic alcohols methanol and ethylene glycol.  Why?  Because Ketones cannot be oxidized to carboxylic acids.

Isopropyl alcohol is metabolized by the alcohol dehydrogenase family of enzymes to acetone. 

Following ingestion, the elimination of acetone is slower than its formation, and this metabolic end-product accumulates.  Acetone itself is a mild CNS depressant and may exacerbate the CNS depression caused by isopropyl alcohol.  It is also responsible for the marked ketosis that is present in most isopropyl alcohol ingestions.

 

KINETICS – Peak serum concentration and clinical effects occur approximately one to two hours after ingestion.

 

CLINICAL FEATURES OF OVERDOSE

Symptoms – nausea, vomiting, and abdominal pain.

Signs – CNS Depressive effects peak within the first hour after ingestion.  Can cause an alteration in mental status similar to that seen in ethanol intoxication.

A fruity breath odor is often perceptible, suggesting acetone accumulation.

Following massive ingestion, signs of shock may be present, as may hematemesis (gastric irritant), pulmonary edema, and hemorrhagic tracheobronchitis.

 

Submitted by Christina Brown.
References: uptodate.com; Trullas JC, Aguilo S, Castro P, Nogue S. Life-threatening isopropyl alcohol intoxication: is hemodialysis really necessary? Vet Hum Toxicol 2004; 46:282. Stremski E, Hennes H. Accidental isopropanol ingestion in children. Pediatr Emerg Care 2000; 16:238. Bekka R, Borron SW, Astier A, et al. Treatment of methanol and isopropanol poisoning with intravenous fomepizole. J Toxicol Clin Toxicol 2001; 39:59.  Su M, Hoffman RS, Nelson LS. Error in an emergency medicine textbook: isopropyl alcohol toxicity. Acad Emerg Med 2002; 9:175.; picture

cannabinoid hyperemesis and…capsaicin?

3 Mar

via a couple EM News articles:

CANNABINOID HYPEREMESIS: QUICK PEARLS:

cyclic vomiting, every few weeks or months

resistant to antiemetics

history of regular cannabis use, usually x years

relief of vomiting/abdominal pain with a hot bath or shower (with resulting compulsive bathing)

episodes ceased when refraining from cannabis use

diagnosis of exclusion

 

INTERESTING BIT ON CAPSAICIN TREATMENT:

TRPV1 receptor in peripheral nervous system – activated by heat >109 F and capsaicin

case series of 7

applied 0.075% capsaicin cream to abdomen

symptoms resolved or drastically diminished in 30-45 min

 

Tiny series, but neat idea.

 

References: EM News article on the syndrome; on capsaicin use; uptodate.com; picture

Management of Cutaneous Anthrax

6 Jan

*Most commonly from contact with infected animals or animal products. Keep bioterrorism in mind and look for evidence of inhalation or GI tract exposure.  

*Incubation period of 1-12 days

***Call the State Department of Health. This is a reportable disease.***

 

Physical exam: Small, painless, pruritic papules -> central vesicle/bulla -> erosion with painless necrotic ulcer/black eschar

 anthrax1 anthrax2

*Oftentimes there is extensive surrounding edema and lymphadenopathy (from toxin release).

*May see systemic signs of fever, malaise, HA. If there are any systemic signs or if the lesions involve the head or neck, treatment must be inpatient. These patients need antitoxin, IV antibiotics, usually an LP, infection control (drainage of effusions…)

 

Diagnosis:

-For vesicular lesions- 2 swabs of fluid from an unopened vesicle. Send 1 for Gram stain/culture and the other for PCR.

-For eschars, the edge should be lifted and 2 swabs rotated underneath. Send 1 for Gram stain/culture and the other for PCR.

-For ulcers, the base of the lesion should be sampled with 2 saline moistened swabs. Send 1 for Gram stain/culture and the other for PCR.

-For all lesions, send a full thickness punch biopsy of the lesion in 10% formalin for histopathology and immunohistochemistry. If the patient is not on antibiotics or has been on antibiotics <24 hours, take a second biopsy for Gram stain, culture, and PCR testing.

 

Isolation: Standard precautions (unless there is continued drainage from wound- then contact precautions).

Treatment: (of cutaneous anthrax without systemic s/sx that does not involve the head or neck)=Generally outpatient.  

7-10 days of ciprofloxacin 500 mg q12 hours

OR doxycycline 100 mg q12 hours OR

clindamycin 600 mg q12.

Follow-up in 1-2 days.

 

Submitted by Heather Groth. 

 

Sources: CDC website, Up-To-Date, Vanderbilt Department of Infectious Disease website

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.