Page 588 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Shock Syndromes 575

Septic Shock tone, bronchoconstriction, angioedema, and urti­
High-dose glucocorticoid therapy in septic shock has caria. 70,156 Anaphylactic shock is typified by hypovolemic
been evaluated in animal experimental studies and human and distributive abnormalities that can be fatal. Therapy
clinical investigations. Several meta-analyses concluded includes fluid resuscitation, antihistamine (both H1 and
H2 receptor antagonists), and epinephrine administra­
that there was no beneficial effect associated with high-
dose steroid therapy for septic shock, many of the clinical tion. Glucocorticoid therapy is routinely recommended
for the treatment of anaphylactic shock but there is little
studies also suggested the possibility that this therapy
could be associated with harm. 21,81 evidence that it is of benefit. Although not expected
to have effects in the acute setting, glucocorticoids are
More recently the syndrome of relative adrenal insuffi­
commonly given in an effort to prevent a recurrence of
ciency (RAI) has been identified in patients with severe
clinical signs and to shorten the clinical course of the dis­
SIRS and sepsis. The hypothalamic-pituitary-adrenal
ease. To date, there are few studies evaluating the benefits
(HPA) axis is crucial for host response to shock. Animals
of glucocorticoid therapy in anaphylaxis. One study of
with inflammatory diseases leading to shock often have
human patients reported that the incidence of biphasic
release of endogenous cortisol early in the course of ill­
or protracted anaphylaxis occurred despite the use of
ness. Cortisol modulates the synthesis and release of 137
glucocorticoid therapy. Systemic glucocorticoids are
proinflammatory and antiinflammatory mediators to
currently recommended for the treatment of anaphylaxis
restrict inflammation to the infected tissues. The cause 31
in veterinary medicine.
of RAI in select patients appears to be multifactorial,
including factors such as vascular or ischemic damage, Hypoadrenocorticism
inflammation, and apoptosis within the HPA axis, use
Hypoadrenocorticism can cause circulatory shock from
of drugs that modify cortisol metabolism, and/or tissue
resistance to corticosteroids. 108,109 RAI may occur in up the combination of hypovolemia and inadequate vasomo­
tor tone. If significant hyperkalemia is present, the resul­
to 70% of people with septic shock and is correlated with
hypotension and death in these patients. 7,64,85,121,127,135 tant bradycardia can also contribute to a decrease in
Preliminary research in dogs, cats, and foals suggests that cardiac output. Shock due to hypoadrenocorticism is a
a similar phenomenon also occurs during critical illness in clear indication for glucocorticoid and mineralocorticoid
these species. 15,20,89,90,111,112 Sepsis-induced RAI in therapy. Adequate fluid resuscitation and medical therapy
humans is typically recognized by a basal cortisol less than as appropriate to lower serum potassium is also essential.
10 mg/dL or a change in cortisol (delta cortisol) of less Dexamethasone is the glucocorticoid therapy of choice
if an ACTH stimulation test needs to be performed
than 9 mg/dL after administration of ACTH. Critically
because it minimally interferes with endogenous cortisol
ill dogs with a delta cortisol less than or equal to 83
measurement. A recommended dose of dexamethasone
nmol/L were almost six times as likely to need vasopres­
sor therapy in one study. 89 The use of physiologic doses of for initial stabilization of patients with hypoadreno­
corticism is 0.1 to 0.2 mg/kg of dexamethasone sodium
hydrocortisone has been found to improve 28-day mor­ 44
phosphate IV. Glucocorticoid therapy does not have to
tality and decrease the duration of vasopressor therapy in
be repeated until 24 hours following this dose and at that
septic humans with a poor response to adrenocorti­
3
cotropic hormone testing. However, a systematic review time it maybe feasible to start oral therapy.
found no clear benefit of steroids on mortality, although BICARBONATE
subgroup analysis of low-dose steroid use suggests a ben­
4
eficial drug effect on short-term mortality. In summary, Metabolic acidosis is likely to be present in all patients
presenting in circulatory shock, secondary to anaerobic
although routine use of hydrocortisone in adults with
metabolism and the subsequent accumulation of lactic
sepsis is still controversial, its use is recommended in adult
acid. The treatment of lactic acidosis with bicarbonate
patients with septic shock that are poorly responsive to
therapy remains controversial. The rationale of treatment
fluid and vasopressor therapy, as well as pediatric patients
with suspected or proven adrenal insufficiency. 4,26,87 is predicated on the notion that having a low pH has neg­
ative effects and hence increasing pH will provide physi­
A reported dose of hydrocortisone that has been used
in dogs for the treatment of RAI is 0.5 mg/kg IV q6h. 105 ologic benefits. Although experimental studies have
demonstrated isolated effects of acidosis, such as
decreases in myocardial contractility and reduced
Anaphylaxis
responsiveness to catecholamines, the results of intact
Anaphylactic or anaphylactoid shock is the result of animal studies are less clear. 48 Human clinical studies have
generalized mast cell and basophil degranulation resulting shown that patients tolerate moderate to severe acidemia
in the release of biochemical and vasoactive substances, without evidence of adverse cardiovascular effects. 158
such as histamine, proinflammatory cytokines, Additionally acidemia may favor oxygen delivery to the
leukotrienes, and tryptase. The clinical consequences tissues by causing a right shift of the oxygen-hemoglobin
include increased vascular permeability, loss of vasomotor dissociation curve allowing for greater oxygen unloading