Page 466 - Clinical Small Animal Internal Medicine

434 Section 5 Critical Care Medicine

a myopathy with increased metabolic heat production. Hyperthermia secondary to seizure activity requires
VetBooks.ir Clinical signs include elevated body temperature and aggressive medical management of the seizure activity
with antiepileptic drugs (diazepam 0.5 mg/kg IV) and
often muscle rigidity. In patients under anesthesia, an
increase in end‐tidal CO 2 may be noted due to the
includes stopping the causative medication, active cool-
increased metabolic rate associated with this condition. active cooling. Treatment of malignant hyperthermia
Various pathologic conditions, including endocrine disor- ing, and administration of dantrolene (2.5–5.0 mg/kg IV).
ders (hyperthyroidism, pheochromocytoma), can induce
an increase in metabolic rate and heat production, as well
as decrease heat loss due to peripheral vasoconstriction. Fever
Hypothalamic lesions that result in an increase in the
temperature set point will create hyperthermia. Hyperthermia in the form of fever is part of the systemic
Prolonged extreme elevations in body temperature can acute phase response to a pathogen or tissue injury and
increase the metabolic rate and demand for oxygen, is aimed at decreasing the ability of infectious agents to
water, and calories that may exceed the body’s ability to replicate and survive. The response may be triggered by
supply them. When this occurs, protein denaturation a variety of infectious agents including bacteria, fungi,
occurs and resulting cellular dysfunction is manifested and viruses, as well as tissue injury from trauma or sur-
as cardiac arrhythmias, liver dysfunction, kidney failure, gery. Neoplastic cells are also capable of inducing fever.
and damage to the gastrointestinal barrier with second- A substance that is created by the body and induces fever
ary bacterial translocation. Acid–base and electrolyte is an endogenous pyrogen, the most significant of which
derangements occur due to dysfunction at the cellular are the cytokines interleukin (IL)‐1, Il‐6, and tumor
and organ level. Muscle damage from high temperatures necrosis factor (TNF)‐alpha. A substance released by an
and hypoxia causes rhabdomyolysis, hyperkalemia, and infectious agent that induces fever is known as an exog-
myoglobinuria, leading to further renal injury. Significant enous pyrogen and includes lipopolysaccharide (LPS)
alterations in systemic coagulation manifest as dissemi- of gram‐negative bacterial cell walls. LPS and other
nated intravascular coagulation (DIC) with thrombosis exogenous pyrogens bind to immune cells and result in
adding to organ dysfunction. Consumption of clotting cytokine release and initiate the acute phase response.
factors results in inappropriate bleeding that may produce Infectious agents also create tissue damage that leads to
clinically significant anemia. the release of cytokines. Once released, cytokines stim-
ulate the arachidonic acid pathway and result in the
Treatment production of prostaglandin‐E 2 (PGE 2 ). PGE 2 is the main
mediator of the fever response through its action on the
Treatment of hyperthermia should be directed at cor- hypothalamus that results in vasoconstriction to prevent
recting the underlying cause and returning the body heat loss and catecholamine release (among other mech-
temperature to normal through the use of active cooling. anisms) to increase thermogenesis.
Active cooling techniques include placing the patient in The cause of fever may be obvious based on history
front of a fan to improve convective heat transfer, removing and physical exam, as in the case of an infected wound or
bedding to allow contact with cool cage or floor surfaces surgical site, or an abscess from a bite wound. If not
to maximize conductive heat loss, and application of readily apparent, an extensive work‐up may be required
alcohol to the foot pads to enhance evaporative heat to identify the underlying cause. A tiered approach to
dissipation. These techniques are generally sufficient for working up a fever is often proposed, starting with a
treatment of hyperthermia of less than 41 °C (106 °F) and minimum database including complete blood count,
should be started on animals with hyperthermia greater chemistry profile, and urinalysis. Thoracic and abdomi-
than 40 °C (104 °F). If these mechanisms are ineffective or nal radiographs with ultrasound are also often included
if hyperthermia is more severe, then dousing the patient in the initial work‐up. If these tests do not provide a
(wet to the skin, not just the hair coat) in cool water and diagnosis, further diagnostics including relevant
placing them in front of a fan is the best way to transfer infectious disease titers (based on geographic area),
heat from the core to the skin and subsequently to the urine culture, blood cultures, echocardiogram, joint
environment. Ice water should be avoided as it will taps, and cerebrospinal fluid analysis may be required.
induce peripheral vasoconstriction and inhibit heat
transfer from the skin and delay core cooling. Application Treatment
of ice water may also induce shivering which can result in
heat generation. Cooling should be closely monitored Identifying and eliminating the cause of true fever is the
and active cooling stopped when the core body tempera- mainstay of treatment. Therapeutic treatment with IV
ture is still above 39 °C (102.2 °F) fluids to maintain hydration and electrolyte balance may