Dermatologic
- Mees lines:
- Arsenic
- Thallium
- Chemotherapy agents
- Radiation
- Bullae:
- Barbiturates
- Carbon monoxide
- Captopril
- Flushed or red appearance:
- Anticholinergics
- Disulfiram reactions
- Niacin
- Boric acid
- Scombroid poisoning
- Monosodium glutamate
- Carbon monoxide (frequently postmortem)
- Cyanide (rare)
- Vancomycin
- Blue skin:
- Ergotamines
- Methemoglobinemia from:
- Nitrite
- Nitrate
- Dapsone
- Aniline dye
- Phenazopyridine
- Benzocaine
- Chloroquine
- Pseudocyanosis from:
- Chlorpromazine
- Amiodarone
- Minocycline
- Silver (argyria)
- Gold (chrysiasis)
ESSENTIAL WORKUP
Depends on ingested substance:
- CBC
- Electrolytes, BUN, creatinine, glucose
- Urinalysis
- Arterial blood gas, venous blood gas
- Carboxyhemoglobin, methemoglobin levels
- Toxicology screen
- Aspirin and Acetaminophen level
- Prothrombin time
- Liver function tests
DIAGNOSIS TESTS & NTERPRETATION
- Anion gap acidosis:
Mnemonic:
A CAT MUD PILES (encompasses a limited number of common causes):
- A
lcohol ketoacidosis
- C
O/cyanide
- A
cetaminophen in fulminant hepatic failure
- T
oluene
- M
ethanol
- U
remia
- D
iabetic ketoacidosis
- P
araldehyde, phenformin/metformin
- I
ron, isoniazid
- L
actic acidosis
- E
thylene glycol
- S
alicylates, sodium azide, hydrogen sulfide
- Increased osmolar gap:
- Methanol
- Ethylene glycol
- Isopropyl alcohol
- Ethanol
- Acetone
- Glycerol
- Mannitol
- Glycine
TREATMENT
INITIAL STABILIZATION/THERAPY
ABCs
ED TREATMENT/PROCEDURES
Depends on ingested substance (see Poisoning; Poisoning, Gastric Decontamination)
PEARLS AND PITFALLS
- Obtain appropriate lab tests.
- Recognize signs and symptoms and lab clues to the toxidromes.
ADDITIONAL READING
- Boyer EW, Shannon M. The serotonin syndrome.
N Engl J Med
. 2005;352:1112–1120.
- Nelson L, Lewin N, Howland MA, et al.
Goldfrank’s Toxicologic Emergencies.
9th ed. New York, NY: McGraw-Hill; 2010.
- Weatherald J, Marrie TJ. Pseudocyanosis: Drug-induced skin hyperpigmentation can mimic cyanosis.
Am J Med
. 2008;121(5):385–386.
See Also (Topic, Algorithm, Electronic Media Element)
- Poisoning
- Poisoning, Gastric Decontamination
CODES
ICD9
- 971.0 Poisoning by parasympathomimetics (cholinergics)
- 971.1 Poisoning by parasympatholytics (anticholinergics and antimuscarinics) and spasmolytics
- 971.2 Poisoning by sympathomimetics [adrenergics]
ICD10
- T44.1X1A Poisoning by oth parasympath, accidental, init
- T44.3X1A Poisoning by oth parasympath and spasmolytics, acc, init
- T44.901A Poisn by unsp drugs aff the autonm nervous sys, acc, init
POLIO
Philip Shayne
•
Marie Carmelle Tabuteau
BASICS
DESCRIPTION
- Caused by poliovirus infection
- Incubation period 7–14 days
- Duration <1 wk
- Clinical manifestations are defined as follows:
- Subclinical (i.e., not apparent) 90–95%
- Abortive poliomyelitis 4–8%:
- Clinically indistinct from many other viral infections (fever, myalgias, malaise)
- Only suspected to be polio during an epidemic
- Nonparalytic poliomyelitis 1–2%:
- Differs from abortive poliomyelitis by the presence of meningeal irritation
- Course similar to any aseptic meningitis
- Paralytic poliomyelitis 0.1%, which is further subdivided:
- Spinal paralytic poliomyelitis (frank polio)
- Bulbar paralytic poliomyelitis (10% of paralytic polio): Paralysis of muscle groups innervated by cranial nerves; involves the circulatory and respiratory centers of the medulla with high mortality
- Mixed bulbospinal poliomyelitis
- Postpoliomyelitis syndrome:
- New onset of increased muscle weakness, pain, and focal or generalized atrophy
- Occurs 8–70 yr after the active illness, usually in the previously affected limb
- Risk factors include age at time of infection, extent of recovery and female sex (increased risk with better recovery)
- Gradual progression
ETIOLOGY
- Polioviruses:
- Picornaviruses
- Small, nonenveloped RNA viruses of the enterovirus genera
- 3 subtypes: 1, 2, 3
- Fecal–oral route transmission
- Enters through oral cavity
- Replicates in pharynx, GI tract, and lymphatics
- Humans are the only natural host and reservoir
- Poliovirus selectively destroys motor and autonomic neurons
- Natural (wild) virus has been completely eliminated in US since 1979
- Oral poliovirus vaccine (OPV):
- Accounts for only poliomyelitis seen in US
- 8–10 cases/yr of vaccine-associated paralytic poliomyelitis (VAP): Neurovirulent conversion of vaccine virus; decreased since widespread use of inactivated poliovirus vaccine (IPV)
- VAP occurs in poorly immunized regions by acquiring properties of wild-type virus.
- There has been a recent increase in some third word countries
DIAGNOSIS
SIGNS AND SYMPTOMS
- Primarily asymptomatic
- Viral symptoms: Fever, headache, malaise. Respiratory symptoms: Sore throat, fatigue GI symptoms: Nausea, vomiting
- Nonparalytic aseptic meningitis: Stiff neck, and or back
- Muscle pain and weakness
- Progressive weakness for <1 wk:
- Dysphagia and dysarthria with bulbar involvement
History
- Vaccination history
- History of prior polio infection
- Recent exposure to individual vaccinated with OPV
- Recent travel to endemic countries (Nigeria, Pakistan, India, Afghanistan)
- Comorbid conditions affecting immunocompetence especially B-lymphocyte disorders (e.g., hypogammaglobulinemia and agammaglobulinemia)
Physical-Exam
- Fever (37°C –39°C)
- Headache, photophobia
- Nuchal rigidity
- Neurologic changes:
- Muscle soreness that becomes severe muscle spasm, progressing rapidly to spotty flaccid weakness and paralysis
- Asymmetric paralysis more prominent in the lower than the upper extremities
- Urinary retention (50% of paralytic cases)
- Reflexes initially hyperactive, then absent
- Apprehensive and irritable, occasionally drowsy
- No sensory loss associated with the motor deficit