Archie, a 1-year 2-month-old male intact Goldendoodle weighing 12.8 kg, presented to Gulf Coast Veterinary Specialist Emergency Services after suffering from heat stroke at a pet sitting service. Previously healthy, fully vaccinated, and on preventative medications, Archie was found unresponsive when the air conditioning system failed, affecting a total of 7 dogs. He was immediately hosed down and taken to the emergency room.
On presentation, Archie was severely mentally obtunded and neurologically inappropriate. His temperature was 103.3°F, heart rate 190 bpm, respiratory rate 36 rpm and unobtainable blood pressure. Cardiovascular examination revealed tachycardia with no heart murmur, normal rhythm with strong heart sounds, but poor femoral pulses. Respiratory assessment showed tachypnea, cyanotic mucous membranes and normal lung sounds. Neurologically, Archie was sternally recumbent and unable to ambulate. He displayed absent menace response bilaterally, intact palpebral reflexes, miotic pupils, and delirium. He also showed bilateral scleral petechiation and hemorrhage. Additional petechiation was observed on the inner pinna, iris, right ventral abdomen, and under the tail. Archie was severely dehydrated (>10%) with tacky mucous membranes.
Initial diagnostics revealed significant abnormalities that included elevated creatinine (2.8 mg/dL), hypernatremia (174 mmol/L), significant metabolic acidosis (pH 7.15, HCO3 10.7 mmol/L), hemoconcentration (HCT 70.9%), thrombocytopenia (96,000/μL), and hyperlactatemia (4.8 mmol/L). Coagulation testing indicated normal prothrombin time (13 seconds), but abnormal coagulation values in the viscoelastic monitor test (VCM) with prolonged clotting formation time (CFT), decreased alpha angle, and decreased mean clotting firmness (MCF). Thoracic radiographs demonstrated severe unstructured interstitial to alveolar lung pattern in the left caudal lung lobe, with moderate changes in the right caudal and accessory lobes, consistent with non-cardiogenic pulmonary edema (NCPE). Point of care ultrasound showed B-lines in both hemithoraces without effusions.
Initial interventions included IV crystalloid fluids (volume resuscitation and replacement), fresh frozen plasma (FFP), vasopressor therapy (norepinephrine), oxygen supplementation, and various medications including maropitant, pantoprazole, mannitol, antibacterials, and vitamin K.
A central line, urinary catheter and a nasogastric tube were placed once transferred to the Critical Care service.
At the end of day 0, Archie developed a ventricular ectopic rhythm characterized by occasional monomorphic VPC’s.
Archie’s cardiovascular condition worsened overnight as his ventricular arrhythmia turned into ventricular tachycardia (V-tach) with pulse deficits and persistent hypotension. Several antiarrhythmics and a magnesium sulfate IV supplementation were tried to control this V-tach but ultimately it was with a esmolol CRI that his arrhythmia was able to be controlled. Cardioversion to normal sinus rhythm improved his work of breathing (WOB) and blood pressure despite de-escalating vasopressor therapy. Based on his increased WOB and flow needs, oxygen supplementation was increased and maintained at 6L/min.
On day 1, the platelet count was zero. This was concerning and an indicator of the progression of his coagulopathy. Archie evidenced black diarrhea that day, consistent with melena. Barium through his NGT was added to his therapy. Prothrombin time surprisingly remained normal throughout hospitalization.
A urine specific gravity (USG) of 1.043 and UOP below 0.5 ml/kg/hr were observed, indicating ongoing dehydration. In response, IVF therapy was adjusted and increased. Subsequently, the USG improved to 1.036 and UOP to >2 ml/kg/hr within a few hours.
Archie experienced two episodes of regurgitation accompanied by high gastric residual volumes (GRV). These symptoms persisted despite the implementation of multiple interventions. Two different prokinetics were administered to improve gastrointestinal motility. Additionally, small continuous rate infusion (CRI) volumes of liquid diet were provided through a nasogastric tube (NGT). Opioids and high-rate crystalloid IV fluids were discontinued to mitigate potential adverse effects on gastrointestinal function.
Archie experienced intermittent episodes of V-tach early in the night. Esmolol CRI was discontinued, and amiodarone was successfully initiated, controlling the arrhythmia. No further V-tach episodes occurred thereafter.
An echocardiogram and cardiology consultation were scheduled for later that day. The echocardiogram revealed no cardiac related abnormalities of dysfunction, suggesting Archie would not suffer permanent cardiac damage from heat stroke and the possibility of a non-cardiac origin to his ventricular ectopic rhythm. Due to his improvement, amiodarone was gradually decreased, with the intention of transitioning to sotalol the following day. A magnesium sulfate CRI was added to his therapy.
Regarding coagulopathy, there was no further evidence of bleeding or petechiation. Archie’s VCM normalized, and his platelet count increased to 55,500/μL. There had been no recurrence of melena since barium administration.
UOP remained adequate at 1.5-2 ml/kg/hr and the USG stayed in the mid-1.030s. Archie was maintained slightly dehydrated to avoid interstitial fluid overload due to vasculitis.
Major blood work abnormalities were not present, as Archie remained normoglycemic, normokalemic, and normonatremic for the past 48 hours.
Repeat radiographs on 07/02/2024 showed mild to moderate improvement in the unstructured interstitial pattern within the left caudal lung lobe. The unstructured interstitial to alveolar pattern within the right caudal lung lobe demonstrated marked improvement. However, Archie’s WOB (inspiratory phase with increased nasal sounds) increased and remained elevated likely related to rhinitis from the nasal devices (cannula and NGT).
Mild non-regenerative anemia was noted, potentially due to medical vampirism, gastrointestinal losses, coagulopathy and severe inflammatory status.
Barium administration was discontinued due to the resolution of Archie’s melena and episodes of regurgitation, which raised concerns about the potential risk of aspiration. The doses of gastrointestinal prokinetics were maximized to address these issues.
Ventricular tachycardia remained mostly controlled. Amiodarone and magnesium CRI were discontinued in favor of oral sotalol.
Archie’s manual platelet count reached 93K, with no evidence of clinical hypocoagulability. PCV dropped to its lowest at 29%.
Archie experienced persistent regurgitation and high GRVs despite the use of prokinetics and temporary discontinuation of water and liquid food through the NGT. His condition worsened as he began groaning and exhibiting clear signs of abdominal discomfort. Abdominal radiographs and ultrasound were performed, revealing findings consistent with severe edematous pancreatitis, gastric wall edema, severe colitis, and mild peritoneal effusion. In response, all food and water administration through the NGT was halted. The treatment plan was modified by adding dextrose to the IV crystalloids and adjusting the prokinetic regimen to include oral cisapride instead of metoclopramide. Additionally, a single dose of dexamethasone at 0.07 mg/kg was administered intravenously.
Archie’s gastrointestinal signs, abdominal discomfort, GRV’s and anorexia gradually and completely resolved. Similarly, the ventricular arrhythmia and slightly increased WOB also normalized. His CBC, electrolytes and biochemistry were within normal limits apart from mild mixed hepatopathy, mild regenerative anemia and mild thrombocytopenia. Radiographically, the NCPE almost resolved as well. On day 10, Archie was discharged home and continues doing well as of today.
Heat stroke is the most severe form of heat-associated illness in small animals. It can be classified as either exertional, occurring due to overheating during exercise, or non-exertional, also known as classic heat stroke. The pathogenesis and pathophysiology of heat stroke are complex and is characterized by multi-organ dysfunction, with central nervous system (CNS) impairment being a hallmark feature. Major body systems include CNS, cardiovascular, pulmonary, gastrointestinal, coagulation, and renal systems. Treatment involves immediate cooling of the patient and providing aggressive multiapproach supportive care.
In dogs, several factors are associated with a worse prognosis. These include metabolic disturbances such as hypoglycemia, decreased cholesterol, increased bilirubin, and decreased albumin. Other factors include obesity, seizures, and coagulation factor abnormalities, including prolonged PT and aPTT, as well as the presence of nucleated red blood cells, which Archie did not develop. Cardiac issues like ventricular arrhythmias, renal dysfunction, and delayed treatment are additional negative prognostic indicators that were observed in Archie’s case. It is important to note that while Archie exhibited some of these negative prognostic indicators, his condition improved over time and was able to be successfully discharged home.
Our discussion will focus on three relevant points: the development of severe ventricular arrhythmia without echocardiographic evidence of heart disease, the development of severe gastrointestinal/abdominal disease, and the development of noncardiogenic pulmonary edema.
First, the development of severe ventricular arrhythmia without echocardiographic evidence of heart disease is a significant concern in Archie’s case. The progression from single monomorphic VPCs to runs of V-tach necessitated an escalation in antiarrhythmic therapy. Initially, boluses of 2% lidocaine were administered, followed by several other antiarrhythmics and ending with an amiodarone continuous rate infusion (CRI) to control the arrhythmia. We suspect that Archie’s gastrointestinal and abdominal disease played a major role in the development of this ventricular arrhythmia. However, it’s important to note that cardiac insult is also a recognized component of the pathophysiology of heat stroke, which may have contributed to the arrhythmia’s onset and progression.
Second, the severe gastrointestinal/abdominal disease affecting Archie’s stomach, colon, and pancreas is addressed, noting symptoms such as thrombocytopenia, abdominal pain, persistent and refractory regurgitation, anorexia, and ventricular ectopy as logical consequences. The discussion suggests that earlier, more aggressive treatment of Archie’s GI disease might have mitigated some of these complications.
Lastly, Archie presented with noncardiogenic pulmonary edema (NCPE), likely resulting from prolonged exposure to extremely high temperatures. Various mechanisms contribute to NCPE, including low alveolar pressure, increased vascular permeability, increased hydrostatic pressure, or a combination of these factors. Neurogenic edema, an important cause of NCPE in dogs, involves excessive sympathoadrenergic activation. This activation leads to pulmonary venous constriction, shifting blood from the systemic to the pulmonic circulation, increasing pulmonary hydrostatic pressure, and ultimately resulting in edema. Other common causes of neurogenic pulmonary edema in dogs include brain trauma, epileptic seizures, and electrocution. In Archie’s case, the prolonged distress from exposure to extremely high temperatures likely triggered excessive catecholamine release, resulting in NCPE.
