Microsoft word - linklater submersion injury.docx
Andrew Linklater, DVM, DACVECC
Clinical Instructor, Lakeshore Veterinary Specialists
Presented at Leon, Mexico Sept 2012
The incidence of drowning in both veterinary medicine and human medicine
is likely under reported due to natural disasters that occur; however it is a leading cause of accidental death, particularly in young males. It is an uncommon presentation in veterinary medicine (compared to human medicine) likely from veterinary patients’ ability to swim at birth and through life.
Rare case reports and one case series exist in the veterinary literature. One
case report is a gelding that became entangled in a safety line while swimming in a pool, another is of a Golden retriever found in a body of water, and some abuse cases from the UK have been reported. There is one case series presented as an abstract at IVECCS in 2006 of 15 dogs and 1 cat; 5 of the pets developed respiratory failure and 37% were non-survivors. It tended to occur in the warmer months (May-Nov) in 9 natural bodies of water and 5 man made bodies of water (1 was not recorded).
There has been much debate recently regarding appropriate definitions
when it comes to drowning. The definition of drowning is respiratory impairment from submersion or immersion in a liquid medium; generally one is considered a drowning victim when death occurs within the first 24 hours of presentation and considered a near-drowning victim if they survive at least 24 hours. A term of secondary drowning has emerged for patients who die from complications associated with drowning. In general, all categories can be included in the term submersion injury. There are 4 general phases of drowning which include breath holding and swimming motions, aspiration of water with choking and struggling, vomiting (which may or may not occur) and cessation of movement and death.
All mammalian species have a dive reflex that occurs with immersion of the
face and upper body (particularly into cold water) that results in bradycardia, apnea and vasoconstriction of non-essential capillary beds. The reflex is strongly expressed in marine mammals and even in predatory marine birds and penguins, but less so in people and land-mammals. This is a survival reflex designed to decrease blood flow to non-essential portions of the body, decrease metabolic rate (to decrease need for oxygen) and prevent aspiration of fluid.
Much debate has been occurred regarding aspiration of salt-water versus
aspiration of fresh water. Salt water is typically 3-3.5% saline and has a high osmotic gradient (higher than plasma) which when aspirated may result in fluid being moved into the lungs potentially resulting in hypovolemia, hemoconcentration and hypernatremia. Fresh water is hypotonic and when aspirated into the alveoli will be absorbed into the body and potentially result in hypervolemia, hemodilution, hyponatremia and hemolysis. Both fresh and salt water aspiration result in flooding of the alveoli and disruption or dilution of
surfactant, which results in alveolar collapse. Ultimately, this very quickly results in poor gas exchange and very rapid hypoxemia. Currently, it is believed that the volumes required to significantly impact gas exchange and result in death or need for mechanical ventilation (3-4 mL/kg) are substantially smaller than those required to affect blood volume (11 mL/kg) or affect electrolytes (22 mL/kg). Although the metabolic derangements that occur in drowning may not theoretically be present, it certainly warrants monitoring. In addition there is a small percent of submersion injury victims (5-20%) that have “dry drowning”, which does not result in aspiration of fluid or debris into the lungs; these patients may still have non-cardiogenic pulmonary edema that develops.
Given the incidence of drowning in natural bodies of water, I would be remiss
to not discuss hypothermia and it’s impact that it may have. Some have reported that drowning in cold water may potentially increase survival (compared to warm water) as it results in a more profound dive reflex and hypothermia slows metabolism and is potentially neuro-protective; others have indicated that cold water may decrease survival as the rapid heat loss may result in faster fatigue and hyperventilation often occurs (particularly if the face enters the water last) result in faster or more pronounced aspiration of fluid. Ultimately, an ER adage from those practicing in cold environments should always hold true: “one is not dead until they are WARM and dead” indicating that even if life is not immediately evident upon presentation, all effort should be made to resuscitate and warm the patient until death is confirmed (by flat-line EKG, rigor mortis or coagulation of blood in the vessels). Hypothermia if immersion occurs in warm water is a negative prognostic indicator.
Common presenting signs of patients who have suffered submersion injury
include respiratory distress, coughing, cyanosis, apnea, vomiting and neurological abnormalities (from sedation to coma). Thoracic auscultation can be extremely variable from normal to asystole and apnea. In human medicine a grading system from 1 through 6 is often used. Grade 1 is a patient that presents only with coughing and a normal thoracic auscultation. Grade 6 is a patient that presents in cardiopulmonary arrest. The usefulness of such a grading system has not been well established if human or veterinary medicine. Hemodynamic status and neurologic status at presentation to the emergency department appear to be the most valuable prognostic indicators.
The pathophysiology of submersion injury can affect many organ systems.
The first and foremost is the pulmonary system. Aspiration of any type of fluid, with the exception of commercial surfactant and perflorocarbons, result in disruption or dilution of surfactant and flooding of the alveoli. Ultimately this results in pulmonary shunting (blood flowing through the lungs without being oxygenated) and systemic hypoxemia. Aspirated matter may contribute to a chemical or bacterial pneumonia along with obstruction of airways.
Fick’s Law states that diffusion or flow of a gas (oxygen) across a barrier
(alveolar exchange to blood) is dependent upon the surface area of the membrane, the thickness of the membrane, the diffusion coefficient of the gas and the difference in pressure from one side to the other. In submersion injury the surface area may decrease due to collapsed or flooded alveoli, the thickness of the membrane may
change (over time) with development of ARDS or inflammation and the difference in pressure may decrease with non-oxygen rich water flooding the alveoli instead of air. Poor gas exchange in the lungs due to a change in ventilation (V) or blood flow (Q) is often called V/Q mismatch; in the case of submersion injury, the ventilation of the affected alveoli falls to zero (when collapsed or flooded), and subsequently gas flow (movement of oxygen into the pulmonary capillaries from the alveoli) falls to zero.
Obviously the neurological system is rapidly affected with loss of oxygen.
The extent and severity of hypoxic brain injury is dependant upon the duration of hypoxia. The Glasgow Coma Scale (GCS) is often used to determine (stage) the extent of one’s neurological injury, and can be monitored over time for improvement. The reader is referred to other sources for more information on the GSC. Lower GCS scores have been associated with a poorer prognosis in people.
The cardiovascular systems can be affected by submersion injury as well. A
hypothermic, hypoxic and acidemic heart is susceptible to a variety of arrhythmias – many of which may require direct treatment (ie unstable ventricular tachycardia), and others may not (ie, occasional VPC); contractility of the heart may be decreased for a variety of reasons and may require pressor (dobutamine) support. Blood pressure can be affected by electrolytes, change in volume status and condition of the heart as well.
Diagnostics that are warranted depend on the condition of the patient,
however checking a blood gas and electrolyte panel along with PCV/TS is the recommended minimum. One may consider checking a full CBC, chemistry and coagulation panel as well. Hospitalization for monitoring is highly recommended event if the patient presents normal. Radiographs are recommended for any patient with any change in respiratory rate, effort, pattern or abnormal lung auscultation on auscultation. Radiographs should never result in a delay in therapy. One should remember that it may take 24-48 hours for radiographic evidence of pneumonia to be evident. Patterns can be quite variable from focal to diffuse alveolar, insterstitial and even bronchiolar patterns. A transtracheal wash for cytology and culture is indicated particularly if the aspirated fluid may have contained debris.
When a drowning victim is discovered, no delay in intervention should occur.
Owners should be instructed to initiate CPCR on site while transporting to a veterinary facility. Recent changes in the AHA guidelines to start compressions before (or even without) ventilation are not appropriate in a victim believed to have suffered submersion injury.
When a patient presents to the ER veterinarian the goals of treatment are to
maximize oxygenation, resolve blood gas and electrolyte disturbances, maintain cardiac output, minimize neurological damage and monitor temperature.
One can minimize impact of neurological damage by administering oxygen,
monitoring and normalizing blood pressure (with fluids and pressors as indicated), avoid manipulation of the head and neck (including occluding jugular veins) and avoid placement of nasal lines that may cause sneezing. Patients with neurological injury should be placed on an elevated board at 10-15 degrees (head up), glucose should be monitored, and any seizures immediately stopped. If a patient is cold, slow re-warming is indicated, but avoid hyperthermia at all costs. If intracranial
edema is suspected, one should treat acid base and electrolyte abnormalities as indicated, and administer 0.5 g/kg of mannitol slow IV through a filter. Some will advocate the administration of lasix (1-2 mg/kg IV) as well. Normalizing oxygenation (PaO2) and ventilation (PaCO2) are always recommended to minimize neurological injury.
Treatment of cardiovascular abnormalities includes administration of
crystalloids and colloids to maintain IV volume, and monitoring PCV/TS, body weight, central venous pressure, urine output, blood pressure and clinical sings of perfusion. Pressor agents such as dopamine or dobutamine may be indicated in select cases. Rarely, patients may be hypervolemic and diuretics may be indicated.
Oxygenation should be maximized by initially administering flow-by oxygen,
however longer term oxygen may be administered with a hood, mask, or cage; or alternatively nasal, nasopharyngeal or tracheal oxygen supplementation may be used. If this is not sufficient, therapeutic ventilation may be required. Treatment with lasix MAY be helpful if the animal has aspirated or ingested a large quantity of fresh water, but multiple doses should be used with caution as they may worsen acid base or neurologic abnormalities. Mechanical ventilation is indicated with a PaO2 < 60 mmHg (on oxygen from an arterial sample) which is equivalent to a pulse-ox reading of 90% as well as if the PaCO2 is > 60 mmHg or there is a marked increase in work of breathing and exhaustion is imminent. Antibiotics may be used if aspiration of bacteria or debris is suspected, but may not be indicated nor necessary in all cases. The use of artificial surfactant has been reported with limited success; its use in veterinary medicine is typically limited to prematurely born animals (horses) and it’s usefulness is not demonstrated. Likely by the time the surfactant is obtained, it’s use would be of little value.
Prognosis of submersion injury victims is variable. In people, 3 factors have
lead to a 100% mortality rate: submersion for more than 25 min, resuscitation duration of more than 25 min and pulse-less cardiac arrest on hospital presentation. Poorer outcomes have been associated with ventricular tachycardia or fibrillation, fixed pupils, severe acidosis and respiratory arrest in the emergency department. Acute pulmonary edema alone has a lower mortality. Hemodynamic status and neurologic status are predictive of outcome according to a 1996 study—patients arriving comatose in the ICU all died or were vegetative; all patients with a detectable pulse and blood pressure on arrival to the emergency department, regardless of their neurologic status recovered to normal. In animals, a worse prognosis is associated with severe acidosis, requirement for CPCR or mechanical ventilation, but level of consciousness is NOT associated with prognosis.
Along with the submersion injury, one should always be conscientious of the
possibility of concurrent injury. For example, patients may have a medical problem (diabetes, seizures) that may have lead to a collapse event and subsequent submersion injury. Alternatively, some injuries (ie unsuccessfully jumping from a boat to a dock) may result in trauma to the head, spine, abdomen, thorax or limbs. These patients may require further diagnostics (imaging), etc. Concurrent hypothermia is the most common injury that occurs with submersion injury; most bodies of water (natural and man-made) are colder than body temperatures. The Great Lakes average winter temperature is 32 F; in the summer, along the coast,
they may reach into the 60s. Smaller lakes in the winter are just above freezing and the freezing point of salt water is 28 F. Water temperatures just above freezing can result in hypothermia and death within 15 minutes, and temperatures around 50 F can lead to death in one hour. Many complications can occur with hypothermia including hypoxemia, metabolic acidosis, poor GI and splanchnic perfusion, reduced cardiac output, multiple organ failure, reduced renal perfusion, a cold-induced coagulopathy (hyper or hypocoagulable), electrolyte disturbances, etc. Animals with extreme hypothermia may appear dead upon presentation, and extreme vasoconstriction with low heart rates can make pulses absent, and death should be determined with an EKG, evidence of rigor mortis or IV coagulated blood.
Any critically ill animal should have close monitoring and supportive care as
indicated by the patient. I would refer the reader to the author’s chapters in the Merck Veterinary Manual, 10th ed. regarding the Monitoring the Critically Ill Patient for further information. References are available upon request.
E260 Acetic acid [Preservative] [Acidity regulator]E101 Riboflavin (Vitamin B2), formerly called lactoflavin (Vitamin G) [Colouring] E261 Potassium acetate [Preservative] [Acidity regulator]E101a Riboflavin-5'-Phosphate [Colouring] E262 Sodium acetates (i) Sodium acetate (ii) Sodium hydrogen acetate (sodium diacetate) E102 Tartrazine, FD&C Yellow 5 [Colouring] E263 Calcium acetate [Prese
DONCASTER PCT PRESCRIBING NEWSLETTER AUGUST 2008 Stronger warnings recommended for etoricoxib Following a review conducted as part of a licence Etoricoxib must not be used in patients extension application, the European Medicines whose blood pressure is persistently above Agency has recommended that the warnings and 140/90 mmHg contraindications for etoricoxib are strength