Cats are great pretenders. They often do not reveal that things are going wrong until their situation is critical. To complicate matters further, critically ill cats may present with non-textbook clinical signs.

In this lecture of two in the series, we will focus on the diagnosis of shock in cats, the formulation of a feline fluid therapy plan and the importance of monitoring of cats whilst receiving fluid therapy.

Shock can be defined as a reduction in oxygen delivery to tissues, most commonly secondary to reduced tissue perfusion as occurs with hypovolaemia. There are six physical examination findings that reflect tissue perfusion: mentation, heart rate, pulse palpation, mucous membrane colour, capillary refill time and temperature. These perfusion parameters can be used to assess whether a patient is in shock. In situations where tissue perfusion is compromised, alterations to these six physical examination findings occur. Decreased tissue perfusion secondary to a reduction in circulating volume activates the neuro-endocrine system. Activation of the sympathetic branch of the autonomic nervous system (adrenaline/noradrenaline) leads to the classic signs of compensatory shock; tachycardia, hyperdynamic pulses and peripheral vasoconstriction causing the mucous membranes to be pale and the capillary refill time prolonged. This response is mediated by both activation of pressure receptors (baroreceptors) and chemosensors (chemoreceptors) in the great vessels. Unlike dogs, where the sympathetic nervous system predominates in shock, in cats the parasympathetic nervous system (mediated by the vagus nerve) is also activated and this vagal response may blunt any compensatory tachycardic response to shock (Schwartz 1973). Many cats presenting with shock have an inappropriately normal or low heart rate. In the absence of this compensatory response, clinical signs as a result of reduced tissue perfusion are usually more obvious; for example, obtundation/stupor secondary to cerebral hypoperfusion and hypothermia. Hypothermia may also contribute to further lowering of the heart rate. Absence of peripheral pulses (carpal and metatarsal pulses) can be supportive of a diagnosis of hypotension, but peripheral pulse palpation can be difficult in cats and care should be taken not to over-interpret these findings in isolation (Reineke et al. 2016).

A blood pressure should be taken in all cats with clinical signs associated with shock.

In light of their small size Doppler blood pressure measurement or the use of high-definition oscillometric devices are preferred over automated traditional oscillometric devices and these methods should not be used interchangeably (Cerna et al. 2020). Doppler blood pressure measurement only provides one blood pressure measurement, and in cats this value is usually considered to be closer to the mean arterial pressure rather than the systolic blood pressure (Grandy et al. 1992). All blood pressure measurements should be interpreted alongside the cat’s clinical signs and it is important to remember that the blood pressure may be normal in the early phase of shock. Lactate, a product of anaerobic metabolism, is a useful biomarker to help diagnose shock early and may have a prognostic value (Shea et al. 2017).

Common causes of shock in the cat include hypovolaemia (blood loss, or fluid losses—renal or gastrointestinal), sepsis and cardiac causes. Many cats have undiagnosed heart disease and may present with clinical signs of shock with or without signs of congestive heart failure. Point-of-care lung and cardiac ultrasound and electrocardiogram should therefore be performed, if available, to rule out a cardiac cause of shock. Should these tools not be available, given that hypovolaemia is the most common cause of shock, a conservative fluid bolus (5 ml/kg isotonic crystalloid over 5–10 minutes) may be considered. The response to a fluid challenge should be assessed immediately after the bolus has been administered; if no improvement in mentation, heart rate or blood pressure is observed, then further bolus therapy is unlikely to be of benefit.

Severe dehydration can lead to hypovolaemia. Common causes of dehydration, particularly in older cats, include polyuria (excessive urine output) secondary to kidney disease, diabetes mellitus, as well as vomiting and diarrhoea. Clinical signs associated with the dehydration include skin tent, sunken eyes, and dry mucous membranes. Skin turgor is dependent on the amount of subcutaneous fat and elastin, as well as hydration status and many emaciated older cats have a skin tent as a result of reduced fat and elastin in spite of adequate hydration (DiBartola, Bateman 2014). A skin tent, therefore, should be used alongside history and short-term weight changes to reliably estimate their degree of dehydration. A re-hydration plan should be based on calculation of fluid deficit, maintenance fluid therapy and adjusted based on ongoing losses (Box 1).

Regular re-assessment of hydration status and frequent weighing alongside monitoring of outputs should be performed in any cat receiving fluid therapy. In cats with conditions associated with increased urinary losses, such as chronic kidney disease, post-obstructive diuresis and diabetes mellitus, fluid rates may need to be in excess of 10 ml/kg/h. Therefore, measuring urine output using techniques such as urinary catheter placement, weighing litter and bladder volume estimation with ultrasound should be performed to help tailor the fluid plan. High fluid rates can impair the normal concentrating ability of the kidney, which can persist for several days and lead to dehydration and hypernatraemia. It is therefore recommended to taper intravenous fluid therapy slowly over 24–48 hours whilst ensuring the cat has free access to water.

Cats are at a risk of fluid overload secondary to fluid therapy. A weight increase of 5–10% above baseline rehydrated weight is suggestive of fluid overload. Fluid overload has been associated with increased cost and length of hospital length (Ostroski et al. 2017) and therefore steps should be taken to prevent it from occurring. Regular respiratory rate checks and repeated point-of-care assessment of the lungs and heart are recommended to assess for indicators of fluid overload such as an increase in left atrium:aorta size, presence of new B lines (lung rockets) and/or pleural effusion. Intravenous fluid therapy should be stopped if signs of fluid overload occur. Should replacement fluids still be required, oral fluids may be administered.

Cats in shock can present in a variety of ways. Consideration of all physical examination perfusion parameters, alongside blood pressure, will help better recognise shock in cats and its potential cause. Fluid therapy is a key aspect of resuscitation and critical care. However, fluid therapy should be considered and prescribed like a drug. Like all prescription drugs, the potential adverse effects of fluid therapy should be considered alongside its benefits. The response to a fluid bolus in the treatment of hypovolaemic shock should be evaluated immediately after the bolus has finished. Cats receiving intravenous fluid therapy to correct dehydration and replace ongoing losses should be regularly reassessed; this may be as frequent as every 2 hours in patients with dynamic disease.

References

1.  Cerna P, Archontakis PE, Cheuk HO, Gunn-Moore DA. Comparison of Doppler ultrasonic and oscillometric devices (with or without proprietary optimisations) for non-invasive blood pressure measurement in conscious cats. J Feline Med Surg. 2020 Jun 25:1098612X20932407.

2.  DiBartola SP, Bateman S. Chapter 14: Introduction to fluid therapy. In: DiBartola SP, ed. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. Fourth edition. St. Louis, MO: Saunders; 2012:331–350.

3.  Grandy JL, Dunlop CI, Hodgson DS, Curtis CR, Chapman PL. Evaluation of the Doppler ultrasonic method of measuring systolic arterial blood pressure in cats. Am J Vet Res. 1992 Jul;53(7):1166–9.

4.  Ostroski CJ, Drobatz KJ, Reineke EL. Retrospective evaluation of and risk factor analysis for presumed fluid overload in cats with urethral obstruction: 11 cases (2002–2012). J Vet Emerg Crit Care (San Antonio). 2017 Sep;27(5):561–568.

5.  Reineke EL, Rees C, Drobatz KJ. Prediction of systolic blood pressure using peripheral pulse palpation in cats. J Vet Emerg Crit Care (San Antonio). 2016 Jan–Feb;26(1):52–7.

6.  Shea EK, Dombrowski SC, Silverstein DC. Survival analysis of hypotensive cats admitted to an intensive care unit with or without hyperlactatemia: 39 cases (2005–2011). J Am Vet Med Assoc. 2017 Apr 15;250(8):887–893.

7.  Schwartz PJ, Pagani M, Lombardi F, Malliani A, Brown AM. A cardiocardiac sympathovagal reflex in the cat. Circ Res. 1973 Feb;32(2):215–20.