When Seizures Become an Emergency: Managing Complications of Cluster Seizures and Status Epilepticus

Stopping the seizure is only the first step when a dog or cat has prolonged or repeated seizure activity. What happens after sustained muscle and brain activity can be just as clinically important. Hypoglycemia, hyperthermia, rhabdomyolysis, cerebral edema, and even pulmonary complications may develop, requiring active monitoring beyond seizure control. 

Watch for Rising Intracranial Pressure 

Prolonged seizure activity can contribute to neuronal injury, cerebral edema, increased intracranial pressure, and reduced cerebral blood flow. 

A change in mentation accompanied by hypertension and reflexive bradycardia, the Cushing’s response, should raise concern for increased intracranial pressure^[1]. 

Management includes controlling seizure activity and addressing intracranial hypertension. The provided approach includes elevating the head to approximately 30 degrees and using hyperosmolar therapy when indicated. Mannitol (20%) may be administered intravenously through a 0.22-micron in-line filter at 0.5–1 g/kg over 20 minutes. Hypertonic saline is another option in patients who are not severely dehydrated or hypernatremic; 7.5% solution may be given at 4 mL/kg IV over 5–10 minutes, while 3% solution may be given at 5.4 mL/kg over 5–10 minutes^[1]. 

Recheck Glucose After Seizure Control^[1] 

Severe muscle and brain activity can contribute to hypoglycemia. This creates an important diagnostic question: was hypoglycemia responsible for the seizure, or did prolonged seizure activity contribute to the low glucose? 

A 50% dextrose IV bolus diluted 1:2–1:4 with an isotonic crystalloid may be used at 0.25–1 mL/kg. Blood glucose should be reassessed 20–30 minutes later because the effect of dextrose is short-lived. If glucose remains low or low-normal, a 2.5–5% constant-rate infusion may be required. 

Serial glucose measurements after seizure control can help distinguish the underlying cause from a consequence of seizure activity. 

Prolonged Muscle Activity Can Damage the Kidneys 

Rhabdomyolysis is another potential consequence of prolonged seizures. Continued muscle activity can result in myoglobinemia and myoglobinuria, with the potential for renal tubular damage and acute kidney injury^[1]. 

A red urine sample that remains red after centrifugation can indicate myoglobinuria. Creatine kinase (CK) may also increase with substantial rhabdomyolysis and brain injury^[1]. 

When myoglobinemia or myoglobinuria is present, balanced crystalloid IV fluids can support renal blood flow, glomerular filtration, and myoglobin excretion. Serial renal values, electrolytes, urinalysis, and CK should be monitored at least every 24 hours. CK activity can peak within 2–12 hours after injury and may return to the reference range within 24–48 hours after the injury has stopped^[1]. Persistent elevation warrants consideration of ongoing seizure activity or an underlying myopathy. 

Hyperthermia and Hyperlactatemia Need Context 

Seizure activity increases oxygen demand in the brain, heart, and skeletal muscle and can produce type A hyperlactatemia. When the seizure is controlled, lactate typically resolves within an hour without specific treatment^[2]. Persistent hyperlactatemia should prompt consideration of another underlying disease or shock. 

Prolonged muscle contraction can also cause hyperthermia. A rectal temperature above 106°F (41°C) represents severe hyperthermia and warrants active cooling with measures such as fans, water baths and IV fluids. Cooling should stop once the core temperature reaches approximately 103°F (39.4°C) to reduce the risk of rebound hypothermia^[1]. 

Do Not Overlook Respiratory Complications 

Neurogenic pulmonary edema is an uncommon complication of severe or ongoing seizure activity. Increased intracranial pressure can trigger a catecholamine surge, producing vasoconstriction, and increased vascular permeability^[3]. Thoracic radiographs may show a bilateral interstitial-to-alveolar pattern, particularly in the caudodorsal lung fields, although the radiographic pattern may take up to 24 hours to develop. 

Treatment relies on supplemental oxygen as needed, with mechanical ventilation required in severe cases^[3]. The role of furosemide is controversial, and it may not be appropriate as first-line treatment when volume overload is absent^[4]. 

Clinical Bottom Line 

Cluster seizures and status epilepticus require monitoring for systemic and neurologic complications even after visible seizure activity has stopped. Serial assessment of mentation, glucose, temperature, CK, renal parameters, electrolytes and respiratory status can help identify complications early and guide supportive treatment.

References:

1. Munguia GG, Brooks AC, Thomovsky SA, Thomovsky EJ, Rincon A, Johnson PA. Emergency approach to acute seizures in dogs and cats. Veterinary Sciences. 2024 Jun 17;11(6):277. https://www.mdpi.com/2306-7381/11/6/277
2. Vincent JL, Quintairos e Silva A, Couto Jr L, Taccone FS. The value of blood lactate kinetics in critically ill patients: a systematic review. Critical care. 2016 Aug 13;20(1):257. https://link.springer.com/content/pdf/10.1186/s13054-016-1403-5.pdf
3. Unger K, Martin LG. Noncardiogenic pulmonary edema in small animals. Journal of Veterinary Emergency and Critical Care. 2023 Mar;33(2):156-72. https://www.abvp.com/wp-content/uploads/2024/05/2024-05-May-CF-non-cardiogenic-pulm-edema-1.pdf
4. Díaz EA, Sáenz C, Torres D, Silva A, Segnini G. Successful management of pulmonary edema secondary to accidental electrocution in a young dog. BMC Veterinary Research. 2024 Apr 19;20(1):145. https://link.springer.com/content/pdf/10.1186/s12917-024-03982-4.pdf