In this section we will feature our most interesting case of the month.

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“Jack”

Signalment: 6 1/2 YR NM DSH

History: ~2wk history of lethargy; owners now reporting loss of appetite, vomiting and vocalizing when picked up. Hx of feline asthma. Becomes stressed while owners are out of town. Current meds include prednisolone and amoxicillin.

Exam: Presented lethargic, ~8-10% dehydrated, unkempt hair coat, occasional vocalizations, mild gingivitis, tender on abdominal palpation, wt loss.

Diagnostics: Normal WBC on CBC (later elevated to 23k), elevated liver values (ALT 473 U/L), hypokalemia (3.2 mMOL/L), hypophosphatemia (3.0 mg/dl), mild hyperbilirubinemia (1.0 mg/dl) and severe hyperglycemia (425 mg/dl) observed on chemistry analysis. UA revealed concentrated urine (sg 1.044) with severe glucosuria (500 mg/dl) and severe ketonuria. Bilirubin initially normal but elevated to 4.2mg/dl 3 days after admission.

Diagnosis: Diabetic Ketoacidosis

Treatment: Following rehydration, a central venous catheter was placed to facilitate blood sugar rechecks. The blood glucose was monitored every 2 hours while a constant rate infusion of insulin was administered. Antibiotics were administered and electrolytes (and phosphorus) were supplemented in the IV fluids. Jack was discharged the following morning and taken to his regular veterinarian for further care. Force feeding was attempted with the regular veterinarian over the next 2 days but was found to be insufficient for Jacks nutritional requirements. Jack was re-admitted to LRH for esophagostomy tube placement and in conjunction with the Animal Diagnostic Clinic, received around the clock intensive care. Episodes of breathing difficulty were noted on readmission but was suspected to be related to the history of asthma. Radiographs were consistent with allergic bronchitis. Bronchodialators were added to treatment plan and an esophageal feeding tube was placed to assist in providing the much needed nutrients for Jack’s recovery. Once Jack became more stable, he was started on an more longer acting insulin (glargine). Jack gained his appetite back and was eventually discharged 11 days after the original diagnosis with a lifelong requirement for injectable insuilin.

Discussion: Diabetic Ketoacidosis (DKA) is a life threatening disease that occurs as a complication of diabetes from a prolonged deficiency of insulin. The purpose of insulin is to “drive” glucose into the cells so that it may be utilized as an energy source. When cells lack sufficient amounts of glucose, the body shifts to an alternate form of metabolism that results in formation of ketone bodies. Stress hormones have also been implicated in promoting the ketone body production and together will lead to metabolic acidosis (elevated pH of the blood). Hyperglycemia (high blood glucose) eventually leads to dehydration by promoting diuresis by the kidneys.

Signs: Presenting symptoms include polyuria (increased urinations), polydipsia (increased drinking), weight loss, vomiting, weakness, mental dullness, and collapse. Initially with diabetes, a voracious appetite is sometimes recognized in the face of weight loss. DKA often occurs in older male cats (>8yrs) and middle age female dogs (~7-9yrs). Pets can often present with concurrent disease processes such as pancreatitis, urinary tract infections, skin infections, kidney disease, etc..

Diagnosis: Hyperglycemia (blood sugar often >400 mg/dl), glucosuria (glucose in urine) and ketonuria (ketones in urine).

Treatment: Intravenous fluid therapy, electrolyte supplementation and eventually insulin therapy are provided around the clock to correct the metabolic derangements. The goal is to convert the DKA patient into a more stable diabetic situation that can be managed as an outpatient. CRI (constant rate infusion) insulin is started once the hydration level of the pet has improved. Central venous lines are placed to facilitate ease of monitoring the blood glucose and electrolytes as samples can often be needed every 1-2 hours for several days. Newer technology is becoming available that will allow us to continuously monitor the body glucose levels. Nutritional support is often necessary and may require esophagostomy or a gastric tube placement. These tubes provide a manner in which to administer the much needed nutrition to promote a more rapid return of normal energy metabolism. These tubes are tolerated quite well and can also be used at home during the recovery process.

24-hour critical care facilities are best utilized for managing these cases due to the constant requirement of medical attention and monitoring.

Prognosis: DKA is a manageable complication but often requires several days of continuous intensive care and hospitalization. Most DKA patients are discharged ~5-7 days after diagnosis unless some other disease process complications are encountered such as kidney failure, liver disease or pancreatitis. Once discharged, the pet will be placed on daily insulin injections which are quite easy to administer for most pets. The regular veterinarian will often request weekly checkups for the first month as the pet’s insulin needs are fine tuned.

Footnote: On a very sad note... Jack developed pulmonary histoplasmosis (fungal pneumonia) the following year and passed away on May 3rd, 2007.

All of us at LRH feel very fortunate to have been able to spend just a fraction of his life with him. With the hours all of us spent with Jack added up…he really found a way into all of our hearts. He remained quite vocal in the ICU throughout his stay (obviously had a lot of things to say to us) and his very unique personality remained quite evident even during his most ill moments. We will miss you Jack.

Histoplasmosis (Histoplasma capsulatum) is a systemic fungal infection caused by a soil-borne fungus that is endemic in many temperate and subtropical regions of the world. Histoplasma capsulatum is found throughout the United States, Central and South America. In the United States it occurs most commonly in the Ohio, Missouri and Mississippi River valleys. The organism thrives in high nitrogen, moist soil and tends to colonize locations rich in bird or bat feces.

Infection with Histoplasma occurs through inhalation of spores. Uncertainty exists as to whether ingestion will produce clinical disease. Once inhaled, they revert to a yeast phase of the organism and reproduces by budding. Organisms then spread to regional lymph nodes and other organs of the body, such as the liver, spleen, bone marrow, bones, and eyes. Occasionally the skin, gastrointestinal tract, mouth, nose, and central nervous system are also affected. If host immunity is adequate, reproduction stops and healing occurs via formation of granulomas with subsequent calcification. In hosts with an overwhelming infection or some sort of immunodeficiency, the organism will continue to reproduce and eventually result in death. The incubation period is 12 – 16 days.
Diagnosis is often confirmed by cytology. Microscopic visualization of the organism in fluids from the airways (trachea/bronchi) or aspirates from masses, lymph nodes or affected organs can often be seen within inflammatory cells. Although readily available, serologic testing is considered an unreliable test in the cat.

It is believed that many animals in the United States are exposed to histoplasmosis, and probably develop subclinical infections that spontaneously resolve without treatment. Disseminated disease and severe infections are often life threatening.

Signs can include pneumonia, lymph node enlargement, liver/spleen enlargement, abdominal fluid accumulation (ascites), bone lesions, and weight loss.

Cats seem to be fairly susceptible to histoplasmosis. The disease occurs more often in cats than dogs. Prognosis for severely ill or debilitated cats is guarded and response to therapy is slow. Anti-fungal therapy can be required for several months and can be quite costly.