Patient: Lily

Signalment: 7-year-old spayed female DLH

History and presenting complaintLily presented to the emergency service at AVES for severe weakness, dehydration, and emaciation. Lily’s family was moving into their new home on January 4th when she accidentally got out of her new house. Her owner had relentlessly searched for her to no avail until a neighbor spotted her in the neighborhood. When found, Lily was extremely weak and had lost more than half of her body weight. She was unwilling to eat or drink at home. Lily was first brought to another emergency facility where bloodwork showed severe anemia (HCT 13.2%) and elevated hepatobiliary enzymes (ALT 335 U/L, ALP 339 U/L, TBili 1.5 mg/dL). Clotting times were normal. She was blood typed (feline type A) and crossmatched to a unit of blood. Lily was transferred to AVES with her unit of pRBC to continue care.

March 20th, 2024

On presentation, Lily is QDR with severe generalized weakness. Although able to stand, would promptly collapse onto herself. Her BCS was 1-2/9 and she weighed only 2.06 kg. She was estimated to be ~9% dehydrated. POCUS reviewed no free effusion. PCV/TS confirmed severe anemia with a PCV of 12% (TS 7.9 g/dL). Saline agglutination was negative. Initial blood pressure via Doppler ultrasound was 40 mmHg. She was given a crystalloid fluid bolus followed by her pRBC transfusion given quickly over 2 hours. Her blood pressure improved to 95 mmHg and PCV increased to 26%. Whole body radiographs were unremarkable. Blood sample was submitted for CBC with pathology review as well as a tick/flea IFA/PCR panel.

Lily was admitted to the ICU for supportive care and monitoring overnight. She remained weak but QAR and hemodynamically stable.

March 21st, 2024

Lily is QDR to QAR this morning, still systemically weak. Abdominal ultrasound showed a diffusely enlarged hyperechoic liver as well as chronic kidney changes. Given her history and elevated liver enzymes, hepatic lipidosis is suspected. Her PCV remained stable at 26% and lytes showed mild hypokalemia and low-normal phosphorous. In anticipation for refeeding syndrome, KCl was supplemented to her crystalloid fluid. A nasogastric tube was placed to facilitate carefully measured enteral nutrition to reduce risk of severe refeeding syndrome. Enteral nutrition was initiated using Royal Canin Recovery liquid diet at ¼ RER. Iron dextran, cyanocobalamin and pradofloxacin were also added pending her CBC with path review and tick/flea IFA/PCR results.

March 22nd, 2024

Lily is QAR, normotensive, normal vitals. She was noted to take a few licks of a/d overnight. She is more interactive and is showing more personality. PCV stable at 25%. CBC with pathology review results were received and showed a marked normocytic normochromic non-regenerative anemia. Small numbers of Heinz bodies were observed, supportive for oxidative hemolytic anemia. Recheck chemistry panel showed hypophosphatemia of 1.6 mg/dL and improved hepatobiliary enzyme elevation (ALP 235 U/L, ALT 223 U/L and normalized TBili of 0.6 mg/dL). Potassium is within normal range. KCl supplementation was switched to KPhos supplementation with a Phos dose of 0.06 mmol/kg/hr. Due to drop in phosphorus, enteral nutrition was not increased from ¼ RER, though the patient is allowed access to a very small amounts of food to which she is taking a few licks.

March 23rd, 2024

Lily is more vocal and “chatty” today. Potassium slightly decreased to 3.3 mmol/L and Phos increased to 4.7 mg/dL. Her ALT and ALP continue to improve (204 and 180 U/L, respectively). PCV is 22% (TS 6.0 g/dL). KCl 20 mEq/L added and KPhos reduced to 0.04 mmol phos/kg/hr. Enteral nutrition increased to ½ RER.

Lily the cat

Lily the cat


March 24th, 2024

Lily is now eating consistently on her own. She is QAR to BAR, loves attention and “talks” at anyone passing by. Hypokalemia has resolved (3.6 mmol/L) and phosphorus is norml/stable. KCl and KPhos supplementations were discontinued as a trial. Enteral nutrition remained at ½ RER because Lily is eating well on her own and we did not want to overly exceed her RER at this time.

March 25th, 2024

Lily remains a very bright, sweet and chatty patient. She continues to eat with a great appetite. Recheck chemistry showed static hepatobiliary enzymes and minor reductions in potassium and phosphorus (not enough to require parenteral nor enteral supplementation). Discussed with owner the option of a cautious home trial. To err on side of caution, we planned for Lily to return in 2 days for a recheck.

Recheck March 27th, 2024

The owner reports that Lily is doing great at home, eating well and unwilling to leave owner out of sight for fear of being lost again! Recheck PCV was 23% and recheck chemistry showed static hepatobiliary enzymes (ALT 363 U/L, ALP 186 U/L, normal TBili 0.4 mg/dL) and normal phosphorus (3.7 mg/dL) and low normal potassium (3.1 mEq/L). Lily and her owner are to follow up with their pDVM in 2-3 weeks.

Late April 

The owner updated us with a recent picture of Lily at home and stated that Lily continues to do well and has been gaining weight (as well as fur) back!

Lily the cat after treatment

Lily the cat after treatment.

Management of patients with prolonged starvation

Lily is a case of severe prolonged starvation. Nutritional support is important for all patients who have had prolonged (generally considered >3-5 days consuming <80% RER). Before initiating a nutritional plan, all patients must have hydration status and electrolyte and acid-base derangements assessed and treatment started to correct those. Patients should be hemodynamically stable before starting enteral nutrition.

Each patient’s energy requirement should be calculated: RER = 70 x (body weight in kg)0.75.

A feeding tube will need to be selected and placed to facilitate enteral nutrition. In Lily’s case, we selected a nasogastric tube because it can be placed rapidly and easily without the need for general anesthesia.

The Royal Canin Recovery diet was selected for Lily for its higher fat content in addition to being calorically dense.

Lily’s enteral nutrition was started at ¼ RER for the first 1-2 days. We were also cautious in the amount of food she was allowed to eat on her own. This approach is to try to prevent refeeding syndrome.

Refeeding syndrome is a potentially fatal condition that is caused by rapid initiation of refeeding after a prolonged period of malnutrition. Patients that have had little or no energy intake for >10 days are at high risk.

During refeeding, glycemia leads to increased insulin release and decreased glucagon secretion. Insulin stimulates the synthesis of glycogen, fat, and proteins. These processes require phosphate. Insulin stimulates the absorption of potassium into the cells through the Na-K ATPase, which also transports glucose into the cells. Magnesium and phosphate are also taken up into cells. These processes result in a decrease in serum phosphorus, potassium, and magnesium, all of which are already depleted during starvation.

When refeeding a patient with prolonged starvation, it is important to carefully monitor phosphorus, potassium, blood glucose, and magnesium if available (ionized magnesium level monitoring not regularly available for veterinary patients). If hypokalemia and/or hypophosphatemia are noted, supplementation should be made to IV fluids. In severe cases, enteral nutrition may need to be reduced or temporarily discontinued until electrolyte derangements are better controlled.