Igor Yankin

A Tricky Enterococcus

A 7-year-old spayed female Persian cat was presented to an emergency service for evaluation of fever, chronic vomiting, and severe lethargy. On initial examination, the cat was stuporous, with fair femoral pulses, pale pink mucous membranes, moderate dehydration, a body temperature of 104°F (40°C), and a heart rate of 150 beats per minute. The initial work-up suggested septic peritonitis and partial jejunal mechanical obstruction, based on abdominal ultrasound and abdominal fluid cytology. Stabilization included fluid resuscitation and intravenous antibiotics (ampicillin/sulbactam at 30 mg/kg IV q8h and enrofloxacin at 5 mg/kg IV q24h), followed by norepinephrine (0.1 mcg/kg/min) due to persistent arterial hypotension. Three hours after presentation, the cat underwent exploratory laparotomy, which revealed a foreign body in the jejunum causing obstruction and perforation. Post-lavage peritoneal swabs were submitted for culture and sensitivity. The cat received resection and anastomosis, along with JP drain placement. Norepinephrine was discontinued 36 hours post-surgery, and nasogastric tube feeding was initiated shortly thereafter.

Gas in the gastric wall: The Good and the Bad

A 15 year-old neutered male Chihuahua was presented to a university teaching hospital for further evaluation of acute vomiting, anorexia, hyperbilirubinemia and elevated liver enzymes. The abdominal ultrasound was suggestive of acute severe pancreatitis resulting in extrabiliary bile duct obstruction. In addition, the gastric wall contained intramural gas consistent with gastric pneumatosis (Figure 1).

Ugly Twins: Combined HHS + DKA (a Feline Case Study)

A 13 year-old castrated male domestic shorthaired cat (2.72 kg) was presented to the veterinary teaching hospital emergency department for worsening lethargy and weakness. He had been recently diagnosed with diabetes mellitus and was started on PZI insulin at 1 unit twice a day. Historically, the cat was diagnosed with ocular histoplasmosis that was in remission on fluconazole treatment.

Management of Hyperosmolar Hyperglycemic State (HHS) in Dogs and Cats: A Clinical Guideline for Small Animal Practitioners

Introduction

This guideline created by the VETEMCRIT Academy is based on the most current veterinary and human medical literature, encompassing both adult and pediatric research. It was designed as a practical clinical tool for small animal veterinary practitioners.

What is HHS?

HHS (Hyperosmolar Hyperglycemic State) is a form of diabetic crisis characterized by severe hyperglycemia (>600 mg/dL or >33 mmol/L), minimal or absent urine/plasma ketones, and serum osmolality greater than 325 mOsm/kg in dogs or 350 mOsm/kg in cats (Koenig et al. 2022).

Diabetic Ketoacidosis (DKA) and HHS are both forms of diabetic crises. They can be viewed as different manifestations along the same spectrum, as evidenced by the fact that some veterinary and human patients present with a combination of HHS and DKA.

However, there are distinct features of HHS that differentiate it from DKA. Veterinarians must be aware of these differences, as they may impact clinical management.

Avoiding Overcorrection: Rebound Hyperkalemia Awareness

Potassium functions as the primary cation inside cells. More than 95% of the total body potassium resides within the cells. Abnormal serum potassium levels may arise due to disturbances in potassium intake, imbalances in internal potassium distribution, or issues with external potassium excretion.

Changes in how potassium is distributed within cells, such as when ß-adrenergic stimulation (as seen in albuterol toxicosis) prompts the movement of potassium in the liver and muscle cells, are usually temporary. On the other hand, a prolonged lack of potassium intake or excessive potassium loss can lead to sustained hypokalemia.

Even though hypokalemia caused by the shift of potassium within cells is temporary, potassium supplementation may be necessary when hypokalemia is moderate to severe, especially if there are observable symptoms like arrhythmia and/or muscle weakness. However, the rate at which potassium is supplemented may need adjustment to prevent a condition called ‘rebound hyperkalemia,’ which can occur after the cause of the potassium shift is resolved.