Case-1

Clinical Notes: Jess

Jess is a five month old female German Pointer. She presents collapsed, with a history of vomiting and lethargy for the past 3 days.

• Learning Objectives
• Clinical Condition
• Case Management
• Suggested Management Plan for Jess
• Further Reading

Learning Objectives

1. Identification of life-threatening abnormalities in a collapsed patient.
2. Prioritising treatment of abnormalities detected.
3. Arriving at an accurate diagnosis and formulating a long-term care and treatment plan.
4. Understanding the aetiology and management of hypoadrenocorticism.

Clinical Condition

Hypoadrenocorticism can occur as a primary condition due to the atrophy (as a consequence of immune-mediated destruction) of all layers of the adrenal gland. This results in a deficiency of both mineral and glucocorticoid secretion. Secondary adrenocorticial insufficiency may occur where ACTH secretion is abnormally low. This may be due to dysfunction of the hypothylamic-pituatary axis or because of the negative feed back effects of exogenously administered glucocorticoids. Clinical signs are the result of the deficiency of glucocorticoids and mineralocorticoids.

Clinical presentation is very varied. Cases may present with mild, non specific signs such as lethargy, occasional vomiting or anorexia. Some animals will present in a crisis - in a very depressed or in a coma, significantly dehydrated (10-15%) and with cardiac arrhythmias.
Those presenting in a crisis can often be easier to spot and diagnose. Initial suspicion is raised when a patient presents in a state of crisis especially where there is a normal or low heart rate in the face of signs of dehydration and hypovolemia (weak or absent peripheral pulses, slow or absent capillary refill, cold extremities). This low heart rate is due to the cardiac effects of hyperkalemia.

Case Management

Important points in management of collapsed patients

1. Rapid assessment of the patient to identify which body system(s) are primarily involved.
2. Obtaining intravenous access.
3. Characterising arrhythmias detected.
4. Obtaining appropriate laboratory samples before initiating treatment.

Management of cardiovascular collapse

1. Correct identification of the cause of cardiovascular collapse.
2. Appropriately sized intra-venous catheter placement.
3. Rapid infusion of appropriate fluids.
4. Pharmacological intervention to promote cardiac output or treat arrhythmias.

Management of hyperkalemia

1. One or more of the following:
   • Shock rate fluids - Hartmann’s, Ringers or Normal (0.9%) Saline. These all act to dilute the serum potassium level and promote diuresis by increasing the intra-vascular volume. Hartmann’s in the preferred option as it also contains some lactate which after metabolism will act to counteract the acidosis that this patient is suffering from. Normal saline and Ringers will dilute the serum bicarbonate and worsen the acidosis.
   • Intravenous regular (soluble) insulin followed by a bolus of glucose. Insulin acts to cause potassium to move into cells. Glucose must be given concurrently or a dangerous hypoglycaemia will develop. Regular (soluble ) insulin must be used as the rate of onset of action of sub-cutaneously administered insulin will be too slow.
   • A bolus of intravenous glucose and rely on innate insulin production.
   • Intravenous sodium bicarbonate solution. As the bicarbonate ion (-ve) is taken up into cells the potassium ion (+ve) moves into cells to maintain electro-neutrality. The administration of bicarbonate
   • Intravenous calcium solution. Calcium will not lower serum potassium levels, but will antagonise the cardiac membrane effects of hyperkalemia and ‘buy time’ to allow one of the above treatments to lower potassium. This buys you about 20 minutes.
2. Ensure appropriate renal function - monitoring urine output is normally easiest. Place an indwelling catheter and record hourly output. At least 1-2ml/kg/hr should be produced. Below this level is indicative of renal failure. Consider further expansion of the intra-vascular volume, use of diuretics or inotropic support.

Management of hypoadrenocorticism

1. Rapid fluid administration to correct hypovolemia. This needs to be followed by continued fluid therapy to correct dehydration and match ongoing losses.
2. Confirm diagnosis by performing and ACTH stimulation test. This should be preformed before drugs such as prednisolone (which may interfere with the test results) are given.
3. Initiate replacement therapy. During the initial period both mineralocorticoids and glucocorticoids will have to be given. In the maintenance phase mineralocorticoids alone will suffice. Patients should be re-checked regularly to ensure that an appropriate dose is being given. This is most easily achieved by measuring serum electrolytes. Additional glucocorticoid therapy will be necessary during periods of stress in the patient’s life (e.g. elective surgery or illness).

Suggested Management Plan for Jess

1. ABC - Airways, Breathing, Circulation. Identify any abnormalities involving the cardiovascular or respiratory systems. These are the conditions that are most likely to result in the death of your patient. Now consider how you might identify the cause of the abnormalities detected (initially these were bradycardia and poor peripheral perfusion).
2. Either record an ECG or obtain a blood sample primarily for electrolyte measurement. Jumping straight to blood sampling would be acceptable as hyperkalemia is a very significant differential diagnosis as a cause of bradycardia.
3. The ECG in this case showed classical pattern seen with hyperkalemia. The P wave is absent, the T wave is abnormally large in amplitude and narrow (sometimes referred to as a ‘spiked T wave’. The rate is slow, but regular.
4. If not already obtained a blood sample should be collected. At this point rapid assessment of PCV and total protein are useful to assess degree of hypovolemia, the measurement of BUN can indicate if acute renal failure has occurred, and the low sodium and high potassium will point towards hypoadrenocorticism as the aetiology of dogs condition. This should be confirmed by performing an ACTH stimulation test. A full haematology and biochemistry is useful, but can wait.
5. Intravenous access should be obtained and appropriate fluid therapy initiated. This may include a colloid to rapidly expand the circulating volume but what the patient really needs is crystalloids with a high sodium content. In this simulation we did not require a specific treatment for the hyperkalemia (though ‘Life points’ were awarded if an appropriate treatment was given). With hyperkalemia of this severity and the associated ECG and cardiovascular changes it would not be wrong to use any of the above mentioned treatments.
6. Replacement therapy with a glucocorticoid and mineralocorticoid should then be initiated.

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