EVERY MEDICAL TEAM eventually faces the challenge of the lateral recumbent emergency. The patient arrives non-responsive and
acutely down, often with no previous medical history of disease or medications. Patients are often hypotensive and clinical diagnostic samples can be difficult to obtain. In these cases, the hospital team has to move quickly to stabilise the patient, choose their diagnostic protocols, and quickly and efficiently develop a treatment plan. For example, Sarah Connor Smith: one year old, 2.78kg (6.11lb), female Chinese Crested. Sarah presented early one morning non-responsive and lateral recumbent, and was immediately brought into the treatment area and evaluated. On initial examination she was obtund, had a heart rate of 60, a
respiration rate of 20, poor pulses, a subnormal temperature of 36.1°C, and had dilated non-responsive pupils.
What should be done first?
Sarah was placed on oxygen mask, an IV catheter was placed, and emergency bolus of IV fluids was initiated. Her initial emergency bolus was calculated at 250ml for the first hour (90cc/kg/ hr) of 0.9% NaCl. Due to low blood pressure, only a small amount of blood
(0.5cc) could be obtained. A team member went to talk to the client to obtain a medical history.
What medical history questions should be asked in an emergency?
The owner reported that Sarah had three or four episodes of vomiting with no diarrhoea in the last two to three hours. There was not any known dietary indiscretion. She was spayed three weeks ago and did not have any known health problems. She seemed to recover well from the surgery; however, next morning she was very lethargic but was back to normal in 24 hours. The owner had never seen Sarah collapse before. While the technical
team member obtained the final history, initial primary diagnostics were being completed.
What diagnostic testing is necessary?
In this case with such a small amount of blood obtained, the clinical diagnostic included a PCV/TP, blood gas (I-STAT EC-8), a blood film, and blood pressure. Further diagnostic testing would be completed once the patient was more stable. The clinical data obtained are shown in the Table. Sarah’s blood film revealed no
obvious agglutination, changes in the red blood cell population, no obvious spike in white blood cell type or number, and a normal platelet count was appreciated.
What is the patient’s problem
list? What is the next treatment course?
Sarah responded slowly to her initial bolus of fluids in the first 10
minutes. Based on blood work, the problem list included hypoglycaemia, hyponatraemia, hypochloraemia, hyperkalaemia, and azotaemia. Further, based on the blood gas, her blood pH
suggested a moderate to severe acidosis (pH < 7.35); the low pC02 supported a metabolic acidosis. The elevation of the anion gap supported an additional charged ion or toxin that was helping produce the acidosis. Based on these concerns, Sarah was
immediately given a bolus of 25% dextrose – 1cc/pound per hour
(0.45cc/kg/hr); she was given 6cc of 25% dextrose. Further, 5%
dextrose was added to the fluid; emergency fluid bolusing was
maintained at the same rate.
What is the differential? What is the continued treatment plan?
Disease differentials included toxin, juvenile hypoglycaemia, sepsis, liver disease (i.e. porto-caval shunt) and endocrine disease. Based on the presence of a moderate metabolic acidosis with an elevated anion gap, hyperkalaemia and hypoglycaemia, and a Na/K ratio of 22:1, primary hypoadrenocorticism (Addison’s disease) was the primary concern. After the dextrose bolus, Sarah’s pupils began to respond to light and her mentation began to brighten. On her next recheck, her blood pressure was 80/35 MAP 55; her fluids were slowed to 2x/maintenance (360cc/ hr or 15cc/hr). A blood glucose rechecked within the next 20 minutes showed a level of 80mg/dl. Sarah was continued on 5% dextrose and was given a (0.25mg/kg) dose of dexamethasone IV. Her azotaemia and acidosis returned to normal within the first 12 to 24 hours. Her electrolytes
began to stabilise and Na/K levels slowly returned to normal ratios.
Her ACTH response test showed low cortisol levels pre- and post-
ACTH injection. She was diagnosed as having a primary hypoadrenocorticism and started on oral prednisone and DOCP injections. Patients that come in lateral recumbent, hypotensive, in shock, and with no indications on medical history of the cause of the disease process can be very challenging for the medical team and difficult for the client to understand. Medical teams must have the tools and protocols in place to help them gain control of an emergency situation. Although every emergency is different,
some basic tips for this type of emergency are:
- Oxygen is never contraindicated – nothing will die from oxygen supplementation as long as administering the oxygen does not further stress the patient. Oxygen masks, cages, e-collars or even placing anaesthetic tubing near the patient’s face may be sufficient.
- Set the catheter – in most cases, the medical team may only have a small window of success to set an intravenous catheter. If there is any doubt, set the catheter. At points a catheter becomes an excellent port for a smooth euthanasia.
- Clinical diagnostics – do a lot with a little – with today’s technology, a small blood sample can give you a great deal of information. A PCV/ TP, blood gas, glucose, electrolytes, and blood film can show a variety of concerns.
- When in doubt, always suspect hypoglycaemia – although occasionally the severely depressed, lethargic patients can be diabetic ketoacidotic patients, always be suspicious of low blood sugar. Be ready to give an emergency bolus of dextrose – 1cc/pound/hr (0.45cc/kg/ hr) of 25% hourly while the patient is on a 5% dextrose drip.
- Understand blood gas – the presence of a metabolic or respiratory acidosis can quickly help point the medical team to the cause of the problem, the potential prognosis and through serial blood work evaluate the patient’s response to treatment. A few guidelines to help understand acidosis are: (a) Blood pH< 7.35 = acidotic patient (b) A low to normal pC02 = metabolic acidosis/a high pC02 = respiratory acidosis (c) Respiratory acidosis is treated with oxygen and increasing gas exchange in the lungs (d) If there is a metabolic acidosis, look at the anion gap (AG), which is a collection of unmeasured electrolytes in the body. Elevations of AG suggest an added toxin or electrolyte in the brew. Elevations of AG can suggest: i. Diabetes ketoacidosis ii. Lactic acidosis iii. Hypoadrenocorticism iv. Uraemia/kidney Dz v. Toxin (e.g. antifreeze, ethanol, paraldehyde [snail bait]…) (e) As the patient’s blood gas improves, this can suggest a positive response to treatment. 6. Respect the patient’s blood pressure – since hypotension is a large concern in these cases, blood pressure is going to be the indicator of stabilisation. Until systolic pressure > 60mmHG, the patient’s organs are not adequately being perfused. These patients also must have aggressive fluid therapy until normal pressure is restored. 7. Lastly, make sure you get a thorough medical data base when the patient stabilises – many of these cases have severe metabolic upsets that secondary complications of disseminated intravascular haemolysis (DIC), organ dysfunction, or rebound hypertension can occur. With proper preparation, developing emergency clinical and treatment protocols and fully evaluating the emergency patient, many lateral recumbent patients can be stabilised and restored.
