resuscitation in small animals - Maravet

Near Drowning 187
13. Schachter S, Norris CR: Laryngeal paralysis in cats: 16 cases (1990-1999). J Am Vet Med Assoc
216:1100,2000.
14. Smith MM, Gourley 1M, Kurpershoek, et al: Evaluation of a modified castellated laryngofissure for alleviation
of upper airway obstruction in dogs with laryngeal paralysis. J Am Vet Med Assoc 188:1279, 1986.
15. Venker-van Haagen AJ: Diseases of the larynx. Vet Clin NorthAmer (SmAnirn Pract) 22:1155-1172, 1992.
16. White RA, Littlewood SO. Herrtage ME. et al: Outcome of surgery for laryngeal paralysis in four cats.
Vet Rec 118(4):103. 1986.
47. NEAR DROWNING
Linda G. Martin, D.v.M., M.S.
1. Define the various terms that have replaced the term drowning, which refers to a submersion
accident resulting in death.
Immersion syndrome: sudden death after contact with cold water.
Submersion injury: submersion resulting in death within 24 hours ofsubmersion (drowning),
at least temporary survival (near drowning), or water rescue or removal of victim from the water.
Secondary drowning: death from complications of submersion more than 24 hours after
submersion.
2. What causes the vast majority ofdeaths after a near-drowning episode?
Almost all patients who ultimately die do so not because of the pulmonary insult and resulting
hypoxemia but rather because of anoxic brain injury. The degree of central nervous system
insult seems to be the limiting factor for survival. Diffuse anoxic injury to the brain results in intracellular
swelling and increased intracranial pressure.
3. What is the mechanism for fresh water drowning?
Aspiration of fresh water causes inactivation of surfactant, which leads to atelectasis and
ventilation-perfusion mismatch. In addition, water in the alveoli interferes with gas exchange by
diffusion impairment. Once in the alveoli, fresh water tends to move rapidly into the intravascular
space. Depending on the initial volume of aspirated water, intravascular volume may significantly
increase as the fluid shift takes place. In the vast majority of cases, despite the increase in
free water, significant electrolyte disturbances do not occur.
4. What is the mechanism for salt water drowning?
The major pathophysiologic change that accompanies salt water drowning is alveolar flooding.
Hypoxemia develops primarily from inability to oxygenate because of fluid-filled alveoli.
The fluid probably remains in the alveoli longer than fresh water. The increased osmolarity of
salt water predisposes fluid movement from the intravascular space into the alveoli, which results
in decreased blood volume and hypotension. Unlike fresh water, salt water does not interfere
with surfactant production by type II alveolar cells or inactivate surfactant. Therefore, alveolar
collapse is not a predominant feature of salt water drowning.
5. Is it possible for drowning victims not to aspirate significant volumes of water?
Yes. Minute amounts of water drawn into the mouth may cause significant and severe laryngospasm.
Hypoxemia may result from persistent laryngospasm. Further attempts to breathe may
result in negative pressure pulmonary edema secondary to laryngospasm and glottis closure.
6. What other secondary problems may occur in near-drowning victims?
Aspiration of water and hypoxemia may lead to cardiac arrhythmias, myocardial ischemia,
cardiac arrest, acute respiratory distress syndrome, pneumonia, acute renal failure, acute hepatic