Page 310 - WSAVA2018
P. 310

 25-28 September, 2018 | Singapore
Heatstroke complications
Azotemia is a common finding in patients with heatstroke. It results from pre-renal and renal mechanisms, such as severe hypovolemia and direct renal tissue damage leading to tubular necrosis, a frequent finding at necropsy of dogs with heatstroke. Acute kidney injury represents a spectrum of conditions associated with sudden onset of renal parenchymal injury. Heatstroke-associated AKI is likely multifactorial. Such factors include decreased kidney perfusion
due to dehydration and hypovolemia, direct thermal injury, myoglobulinemia due to rhadomyolysis, DIC, endotoxemia and the systemic inflammatory syndrome. Kidney injury may be mild and go unnoticed, but often, failure of the kidneys to meet the excretory, metabolic, and endocrine demands of the body ensues. Kidney function parameters can be classified to those measured routinely (e.g., serum creatinine), those not measured routinely, but are calculated using routine chemistry
(e.g., glomerular filtration rate [GFR] using endogenous creatinine clearance and fractional electrolyte excretion) and unique urinary renal biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL), C-reactive protein (CRP) and retinol-binding protein (RBP). NGAL is a 25 kD protein, covalently bound to neutrophil gelatinase. Normally, its expression and concentration are low; however, its expression is markedly induced when renal tubular epithelial injury occurs, and it is now identified as one of the earliest and most robustly induced proteins in both human and animal patients. RBP is a low molecular weight protein, freely filtered and is completely reabsorbed by renal epithelial tubules, rendering it
a marker of renal tubular function. C-reactive protein (CRP), on the other hand, is a relatively high molecular weight protein, and therefore is normally not filtered through the glomerulus. Thus, its urine concentration reflects changes in glomerular capillary permselectivity characteristics. In this study we have found that renal biomarker analysis, GFR and sodium fractional excretion can identify kidney damage earlier, immediately at presentation and therefore aid the clinicians in the overall assessment of the animal. Nevertheless, the presence of AKI based on the traditional parameters during hospitalization of serum creatinine levels >1.5 mg/dL at 12 and 24 hours after presentation were
found to be independent risk factors for death in dogs with heatstroke. Therefore, careful monitoring of renal function and early intervention are warranted.
Severe hyperthermia may lead to cerebral hypoperfusion, neuronal necrosis, direct vascular damage, cerebral edema, hemorrhage and multifocal vascular thrombosis with tissue infarction that may lead to CNS dysfunction and death. The canine brain is considered more resistant to thermal injury compared to the human brain and other physiological factors, such as respiratory alkalosis, shock and hypoglycemia,may play
a more significant role in the observed CNS clinical signs in canine heatstroke. Thermal and biochemical injury to the pulmonary endothelium may lead to non-cardiogenic pulmonary edema, also known as ARDS. Histopathologic lung lesions in dogs suffering from heatstroke include pulmonary infarcts, marked alveolar hemorrhage or edema.
A few extra-cardiac mechanisms were proposed as contributing processes to the development of cardiac arrhythmias. These included myocardial hypoperfusion, lactic acidosis and electrolyte imbalance and possibly direct thermal injury. Post mortem findings in 11 dogs with heatstroke showed mild to severe subendocardial, myocardial and epicardial hemorrhages and hyperemia in all dogs.(4) These findings suggest that DIC has
a pivotal role in the pathogenesis of the reported cardiac arrhythmias. Antiarrhythmic therapy should be considered, however, only if the patient has related clinical signs.
In humans and experimental studies, marked increases in core temperatures are associated with blood flow redistribution, which is characterized by coetaneous vasodilatation that occurs at the expense of decreased intestinal blood flow. This splanchnic vasoconstriction may cause ischemia and limit local vascular heat exchange, thereby promoting bowel tissue hyperthermia. Both intestinal ischemia and hyperthermia may promote oxidative stress that stimulates cytoskeleton relaxation, thus contributing to the opening of tight junctions and/
or injuries to the epithelium. These morphological and functional changes enhance intestinal permeability, thus facilitating the translocation of bacteria and endotoxins that are normally contained within the intestinal lumen, and subsequently worsening a systemic inflammatory response syndrome that may culminate in multi-organ system failure and death. Gastrointestinal bacterial translocation has not been specifically documented in dogs with naturally-occurring heatstroke; however given the massive hemorrhagic diarrhea and hematemesis
that rapidly ensues in dogs with severe heatstroke, it is reasonable to assume that it is a major contributing factor to SIRS, sepsis and MODS that may occur in severe cases.
In summary, clinicopathological findings in canine heatstroke are mainly related to the primary thermal insult; however, secondary deterioration occurs due to dehydration, shock and a poor perfusion to the tissues. Thus, early diagnosis and intervention are crucial to prevent further multi-organ dysfunction and exacerbation of coagulation abnormalities. Time lag from insult to admission (>1.5 hrs) was a crucial factor for survival in canines suffering from heatstroke.

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