The Flat Cat

Abstract

Aim:

Detailed information regarding the causes and treatment of acute collapse in the cat can be difficult to locate in a single published source. This two-part review aims to provide a logical approach to the clinical assessment and stabilisation of the critically ill collapsed cat.

Practical relevance:

Cats are particularly challenging when presented as emergency patients, often in the later stages of an illness or with a vague history and non-specific signs. The nuances of the critically ill cat are considered, especially for shock and its management.

Clinical challenges:

Shocked cats do not present in the classic stages typically seen in dogs, and the signs are more subtle. Therefore, the clinician must consider whether physical parameters are appropriate for the state and environment of the patient; for example, a normal heart rate in a shocked cat would be considered inappropriate.

Audience:

This review is directed at any veterinarian working with feline patients, and particularly those dealing with emergencies on a regular basis.

Evidence base:

There is an extensive body of published literature, both original studies and textbook chapters, pertaining to the causes and treatment of collapse in the cat. In this article the authors draw on information from original publications, reviews and their clinical experience to provide practical guidance to assist in the emergency setting.

The challenges of collapse in the cat

Collapse can be caused by a bewildering number of different conditions and, therefore, adopting a logical approach to assessment and investigation is essential when presented with a collapsed cat. Cats are particularly challenging in critical care and a number of unique features, including their smaller blood volume, shock response and blood types, mean a different approach is required compared with treating collapsed dogs.^1,2 Specific features of feline patients that should be considered are listed in Table 1. The first step is to rapidly assess the collapsed patient to identify and stabilise any life-threatening abnormalities, and is the focus of this two-part article.

Table 1

Unique features of cats to consider in critical care

Feature	Feline-specific considerations	Clinical significance
Shock	Hyperdynamic compensatory phase of shock including tachycardia and ‘snappy’ pulses is less commonly observed. Hypothermia, hypotension and bradycardia/ normal heart rate are more frequent features^2–4	Consider whether the heart rate in a collapsed or critically ill patient is appropriate. Assess all perfusion parameters together
Vascular volume	Smaller at 66 ml/kg versus 90 ml/kg in dogs¹	Smaller boluses and total doses are used for resuscitative fluid therapy in shock (eg, 5–10 ml/kg bolus, 40–60 ml/kg total dose for crystalloid fluids)
Body surface area	A higher surface area/body mass ratio is a feature of small patients	Cats have increased susceptibility to rapid heat loss and less efficient compensatory heat production³
Shock organ	Considered to be the lungs in cats versus the gastrointestinal tract in dogs; leakage of protein into the alveoli has been documented in experimental models of sepsis^5,6	Frequently re-evaluate the respiratory rate and pattern and reassess lung sounds in critically ill cats; tachypnoea, increased respiratory effort and pulmonary noises (‘harsh’ lung sounds and/or pulmonary crackles) may indicate pulmonary complications of shock, SIRS or sepsis
Occult cardiac disease	Occult cardiomyopathy is not uncommon and may be due to subclinical primary cardiac disease or the consequence of systemic illness (eg, hypertension, hyperthyroidism, severe anaemia)^7–9	Occult cardiac disease increases the risk of volume overload and development of pulmonary oedema ± pleural effusion following intravenous fluid therapy. Frequently reassess the heart and respiratory rate, heart rhythm and pulses, and auscultate for heart murmurs, gallop sounds, arrhythmias and pulmonary crackles in critically ill cats
Susceptibility to volume overload with fluid therapy	Development of pulmonary oedema and pleural effusion is a common complication in cats due to excessive fluid administration. Cats are less tolerant of large fluid loads¹⁰	Risk factors include hypothermia (which blunts the vascular response to fluids in cats), occult cardiac disease, pre-existing pulmonary disease (eg, aspiration pneumonia), SIRS/sepsis, renal failure, acidosis, hypocalcaemia, hypoalbuminaemia, administration of colloids (especially haemoglobin-based oxygen-carrying solutions) and severe anaemia^3,10
Stress hyperglycaemia	Commonly detected in sick or stressed cats due to increased circulating catecholamine levels (eg, ≤16 mmol/l, 285 mg/dl in acute stress)¹¹	Recheck blood glucose levels following a period of acclimatisation to determine if there is a persistent elevation; stress hyperglycaemia is typically transient
Drug metabolism	Reduced capacity for hepatic glucuronidation and deficiency of thiopurine methyltransferase¹²	Reduced hepatic glucuronidation is the reason that paracetamol toxicity occurs at 3–4-fold lower doses in cats versus dogs.¹³ It is also the suspected aetiology of species-specific permethrin intolerance¹⁴
Anaemia	Anaemia of chronic disease is common (typically a mild anaemia). Patients with chronic non-regenerative anaemia due to primary bone marrow disease frequently present with a severely reduced PCV (<10%)¹⁵	Assess PCV in the light of dehydration – it can be overestimated when there is haemoconcentration. Severe anaemia may be associated with cardiac changes leading to increased risk of volume overload – requiring care with fluid administration.⁹ Severity of anaemia on presentation was not found to be associated with survival in a recent study¹⁵
Blood types	Cats have preformed blood type antibodies	Blood typing, and ideally cross-matching, should be performed before any transfusion; administration of incompatible blood is potentially fatal
Constant dietary protein requirement	Inability to down-regulate protein requirements¹⁶	Catabolism of body protein for gluconeogenesis occurs rapidly following a period of anorexia and illness. Assessment of nutritional requirements is a priority following emergency stabilisation and assisted feeding may be necessary in the critically ill patient¹⁷
Hepatic lipidosis	Risk of development in all cats (regardless of body condition) following even short periods of partial anorexia (<1 week)^18,19	Assessment of nutritional requirements is a priority and assisted feeding may be necessary in the critically ill patient
Pain manifestation	Signs are often subtle, including a hunched body position, reduced palpebral fissure, staring coat, lack of interaction, lack of grooming, inappetence, reluctance to move and aggression²⁰	Assessment of response to an ‘analgesic trial’ using a short-acting opioid may be necessary to confirm suspicion of pain. Evaluate for pain using physical examination, heart rate, respiratory rate, rectal temperature and behaviour. Diffuse abdominal pain can be a feature of sepsis, even in the absence of overt abdominal pathology²
Fear aggression	Fearful, stressed and painful cats can sometimes be challenging and even dangerous for personnel to handle; however, fear aggression is an extreme response for a feline patient to mount. Always consider ‘why is the cat demonstrating aggression?’	Efforts should be directed at addressing pain, and minimising excessive handling and stress in anxious cats. Follow the recommendations of the AAFP and ISFM with respect to feline nursing care and handling.^21,22 Consider sedatives carefully for extremely fractious patients²⁰

SIRS = systemic inflammatory response syndrome, PCV = packed cell volume

What causes collapse?

Collapse can be defined as a failure to maintain normal posture and can be associated with or without loss of consciousness. Owners often use terms such as ‘fit’ to describe these episodes, which can imply a particular aetiology. The clinician must ensure this does not mislead them and that they acquire a careful history and description of the event.

Cats with a history of collapse can have three main types of presentation:

Acute collapse;

Episodic collapse;

Apparent collapse (whereby the patient is recumbent and either unable or reluctant to walk).

Some of the important causes of collapse are shown in Table 2.

Table 2

Common causes of collapse

Body system	Disease	Typical form of collapse
		Acute	Episodic	Apparent
Cardiovascular	CHF due to cardiomyopathy	✔
	Arrhythmia	✔	✔
	Pericardial disease causing tamponade	✔
	Arterial thromboembolism	✔
	Shock: hypovolaemic, cardiogenic, obstructive, distributive	✔
Respiratory	Pleural effusion (eg, CHF, pyothorax, haemothorax)	✔
	Asthma	✔	✔
	Pneumothorax	✔
	Airway obstruction: foreign body, tumour, laryngeal paralysis	✔
	Diaphragmatic rupture	✔
Haematological	Severe anaemiaRegenerative:Haemorrhage – Internal (eg, rodenticide toxicity, urinary or gastrointestinal tract haemorrhage) – External (eg, trauma)Haemolysis – Immune-mediated; primary or secondary – Incompatible transfusion – Neonatal isoerythrolysisNon-regenerative:Bone marrow disorder, FeLV infection	✔
	Hyperviscosity: erythrocytosis, hyperproteinaemia	✔
	Methaemoglobinaemia: paracetamol toxicityCarboxyhaemoglobinaemia: smoke inhalation	✔
Metabolic	Hypoglycaemia	✔
	Hypokalaemia, hyperkalaemia	✔
	Hyponatraemia, hypernatraemia	✔
	Hypocalcaemia	✔
	Hypercalcaemia	✔		✔
	Hepatic encephalopathy	✔	✔
	Uraemic encephalopathy	✔
Endocrine	Diabetic ketoacidosis	✔
	Phaeochromocytoma	✔	✔
	Thyroid storm due to acute thyrotoxicosis ± comorbid disease	✔
Gastrointestinal and pancreatic	Gastrointestinal perforation and peritonitis	✔
	Acute pancreatitis and associated metabolic complications	✔
	Gastrointestinal obstruction	✔
Central nervous system – brain and upper motor neurons	Seizures	✔	✔
	Central vestibular disease	✔
	Brain and spinal neoplasia	✔
	Ischaemic myelopathy	✔
	Head trauma	✔
Peripheral nervous system and musculoskeletal system	Peripheral vestibular disease	✔		✔
	Polymyopathy (eg, hypokalaemic myopathy of Burmese cats), Toxoplasma gondii myositis		✔	✔
	Polyneuropathy (eg, diabetic), inherited hyperchylonmicronaemia			✔
	Myasthenia gravis	✔		✔
	Intervertebral disc disease	✔		✔
	Severe orthopaedic pain, fracture	✔		✔
Toxins and drugs	Organophosphate and carbamate insecticides, permethrin, ethylene glycol, paracetamol, lilies, rodenticides	✔
	Hypotensive drugs: eg, β-blockers, calcium channel blockers, α₂ agonists, phenothiazines, diuretics	✔
Miscellaneous	Sepsis, SIRS	✔
	Anaphylaxis	✔
	Severe pain	✔		✔

Adapted from the BSAVA manual of feline practice: a foundation manual (in press)

CHF = congestive heart failure, FeLV = feline leukaemia virus, SIRS = systemic inflammatory response syndrome

How does the collapsed cat differ from the collapsed dog?

Signs of illness including shock are typically more subtle in cats and it is common for cats to be presented in the later stages of an illness, with an acute decompensation of a chronic disease. Frequently the owner actually perceives only a short period of ill health – an example might be a dyspnoeic cat presenting in fulminant congestive heart failure. Cats often do not show the same clinical signs as dogs with the same disease and a particular example of this is acute pancreatitis. Dogs typically present with gastrointestinal signs and abdominal pain, whereas cats may present with anorexia, severe hypotension and hypothermia but without obvious pain and other gastrointestinal signs.²³

The typical clinical presentation of shock is often not seen in cats either – for example, bradycardia may feature instead of a compensatory tachycardia. Furthermore, the approach to managing shock needs to be modified due to smaller blood volumes compared with dogs, an essential requirement to address hypothermia and the possibility of occult cardiomyopathy.^1–4,7,8 Finally, cats often require support and stabilisation for more extended periods than their canine counterparts.

Clinical signs of shock

Shock is frequently encountered in the acutely collapsed cat. Shock is a condition of imbalance between oxygen delivery and oxygen consumption, and can be divided into four main categories:

Hypovolaemic shock;

Cardiogenic shock;

Obstructive shock;

Distributive (hyperdynamic) shock.

Hypovolaemic and cardiogenic shock are more commonly encountered in feline practice and an individual cat may have more than one mechanism contributing to compromised perfusion. Common causes of shock are shown in the box on the right.

Shocked cats are extremely challenging and there are some important differences to be aware of compared with dogs. A dog in hypovolaemic shock would be tachycardic until entering decompensated terminal shock. However, it is more common for cats to be bradycardic or to have a normal heart rate (this could be considered a relative bradycardia in a hypotensive patient). Signs of hyperdynamic shock typically associated with sepsis such as hyperaemic congested mucous membranes and ‘bounding’ peripheral pulses are not often seen in the cat.² Hypothermia is common in shocked cats and blunts the normal vasoconstrictive response to hypovolaemia. This, in turn, increases the risk of fluid overload if feline patients are aggressively volume resuscitated while hypothermic.^2,3

Furthermore, occult cardiac disease is common in cats due to primary cardiomyopathy or secondary to systemic illness; therefore, careful auscultation prior to, during and following fluid therapy is essential to aid early identification of volume overload before the cat decompensates into overt congestive heart failure.^7–9 The clinician should carefully evaluate the cat for the presence of a heart murmur, gallop rhythm, arrhythmia, pulmonary rales and crackles before, during and after treatment of shock. It should be remembered that absence of a heart murmur on auscultation does not fully exclude the possibility of occult cardiomyopathy.⁸

Treatment of shock needs to be modified for cats, using smaller fluid boluses in view of the smaller blood volume of a cat relative to the dog, the frequent existence of occult cardiac disease and greater susceptibility to fluid volume overload. Cats are significantly less tolerant of fluid loads, with a tendency to develop pulmonary oedema and/or pleural effusion, which may be due to pre-existing issues with cardiopulmonary function and/or a complication of hypothermia or a consequence of shock leading to multiple organ failure (see Table 1 for risk factors for volume overload).^3,9,10 The lungs are considered to be the ‘shock organ’ in cats and are particularly vulnerable to injury during sepsis.^2,5 Acute lung injury and acute respiratory distress syndrome can be associated with SIRS or sepsis and can lead to alveolar damage and infiltration, causing progressive hypoxaemia, tachypnoea, dyspnoea and cyanosis.^24,25

Practical approach to the emergency patient

The successful management of an acutely collapsed cat involves the following steps:

Perform rapid physical assessment including thorough cardiac evaluation to try to identify occult cardiac disease;

Obtain vascular access and begin fluid resuscitation (provided no congestive heart failure);

Acquire emergency database;

Identify life-threatening abnormalities based on physical and laboratory evaluation;

Form a brief problem list and prioritise problems;

Address critical problems and provide supportive care to stabilise the patient;

Complete a detailed physical examination including re-evaluation of vital parameters (and further cardiac evaluation to detect occult cardiac disease) to assess the response to treatment, and obtain a history.

Be prepared!

In order to complete this process efficiently, all members of the veterinary team should be familiar with the steps that will need to be taken in the emergency situation and the specific tasks they will perform. An open area is ideally used for assessment and stabilisation, preferably with access to oxygen and a ‘crash’ kit, so that the team are prepared to perform cardiopulmonary resuscitation if necessary. Monitoring equipment should be easily accessible. Ideally, this would include an electrocardiograph, non-invasive blood pressure monitor, pulse oximeter and capnograph; however, much can still be achieved with careful monitoring using clinical observations alone.

Initial assessment

Initial assessment involves a rapid examination of vital organ function, focusing on the cardiovascular, respiratory and neurological systems. This should quickly determine whether the cat is in shock. Baseline vital parameters should be recorded (temperature, pulse, respiratory rate). It is helpful for an assistant (if available) to obtain owner consent and a brief history, to allow the vet to focus on the patient. Useful questions to consider are listed below.

A methodical examination ensures that major systems are not overlooked. Immediately consider if the cat is responsive, breathing and whether it has palpable pulses or heart beat to aid identification of cardiopulmonary arrest. This is similar to the traditional ABC (airway, breathing, circulation) approach. If a cardiopulmonary arrest is identified, the key basic life support recommendations from the RECOVER (Reassessment Campaign on Veterinary Resuscitation) initiative should be followed (see above).²⁶ If cardiopulmonary arrest is not detected, continue to the preliminary examination.²⁶

Preliminary examination

Cardiovascular system

Assess markers of peripheral perfusion:

– Mucous membrane colour; pallor may be due to vasoconstriction as a result of shock or anaemia;

– Capillary refill time;

– Peripheral and femoral artery pulse quality and rate (auscultate the heart simultaneously to detect pulse deficits).

Assess for signs of cardiac disease:

– Does the cat have a heart murmur, gallop rhythm or dysrhythmia?

– Are the heart sounds muffled? This could be consistent with a pleural or pericardial effusion.

Respiratory system

Assess breathing rate, pattern and effort.

Assess for upper respiratory tract noise, wheezes, pulmonary crackles, or loss of lung sounds over the thorax – such findings will help to localise the affected area of the respiratory tract if dyspnoea is a presenting feature.

Is the cranial thorax compressible? Loss of compliance could be due to a space-occupying lesion/mass, pleural effusion or pneumothorax.

Is percussion of the thorax normal? Increased resonance may suggest pneumothorax; decreased resonance could be due to pleural fluid, pulmonary consolidation or a mass.

Neurological system

Assess mentation – is the cat normal, obtunded (depressed), stuporous or comatose?

If the cat is conscious, evaluate its ability to ambulate and the pedal withdrawal response.

Abdominal palpation

Perform a rapid check for ascites, bladder size, organomegaly, masses and abdominal pain.

Rectal temperature

Hypothermia <37°C (98.6°F).

Hyperthermia >39.2°C (102.5°F).

Hydration status

Assess mucous membranes and skin turgor.

Securing intravenous access

Placement of an intravenous (IV) catheter is a priority in order to facilitate fluid and drug therapy, and to be prepared should a cardiopulmonary arrest occur. The largest bore catheter possible should be placed (ideally 22 gauge). Peripheral vasoconstriction in shock often makes placement of a catheter more challenging; if the cephalic vein is not easily visualised it can be helpful to clip a larger area of fur and try to follow the path of the vein from the more distal bifurcation (Figure 1). Application of a tourniquet proximally for 2–3 mins may aid identification of the vein. Alternatively consider placing the catheter in the medial saphenous vein, which is often easier to see (and a suitable site for a long-stay catheter) (Figure 2).

Figure 1

Cephalic vein outlined to show the distal bifurcation

Figure 2

Medial saphenous vein – a useful site for intravenous catheterisation as this vessel is usually easily visualised

If peripheral vein cannulation cannot be achieved, placement of a central venous catheter into the jugular vein is the next step. The Seldinger technique is used and is easily learnt. The technique involves the placement of a short IV catheter into the jugular vein initially to act as a conduit for the passage of a guide wire into the vein. The short catheter is removed, leaving the wire in place. The wire then facilitates the passage of a longer catheter. The longer catheter can be placed to allow central venous pressure (CVP) measurement and can permit collection of blood samples, and administration of more hypertonic fluids among others. These catheters can be single lumen or multi-lumen; the latter are particularly useful for patients receiving fluid therapy that also require frequent blood sampling and CVP measurement. Note that central venous catheters are contraindicated in cats with venous thrombosis, bleeding disorders or elevated intracranial pressure.

Veterinary kits (Figure 3) are available containing the required equipment (4.5 French gauge, 6 or 8 cm dual or triple lumen jugular catheters are suitable). If unavailable, a standard over-the-needle catheter can be placed in the jugular vein; alternatively intraosseous catheterisation can be used for vascular access. The Seldinger technique can also be used to place a long catheter into the medial saphenous vein, which can be useful for longer-term (eg, > 48h) venous access.

Figure 3

Jugular catheter kit showing a dual lumen 4.5 Fr 6 cm catheter (Vygon). Courtesy of Dr Séverine Tasker, University of Bristol

Intraosseous catheterisation (see below) is useful in patients where peripheral or central venous access has not been obtained, but is best replaced by peripheral access once the cat has been volume expanded as intraosseous catheters can be uncomfortable once the cat is mobile.

Fluid therapy – which fluid, how much and how fast?

In cases of hypovolaemic, obstructive or distributive shock, resuscitative fluid therapy is the first step in stabilising the cat by restoring the circulating volume to improve tissue perfusion globally. Fluid therapy is contraindicated in patients with congestive heart failure.

The blood volume of a cat is 66 ml/kg, which is less than that of the dog (90 ml/kg). This is important to remember when performing resuscitative fluid therapy, particularly given the cat’s sensitivity to volume overload; shock doses of crystalloids and colloids are therefore smaller than those used in dogs (40–60 ml/kg and 10–20 ml/kg, respectively).^1,29 Overly aggressive fluid therapy should be avoided and a careful balance must be struck between administering sufficient fluid to improve perfusion while preventing volume overload. If the cat is fluid overloaded, pulmonary and pleural fluid may accumulate and result in further hypoxia (Figure 4).

Figure 4

Dorsoventral radiograph of a cat demonstrating features consistent with volume overload; there is a small pleural effusion with retraction of the pulmonary lobes from the thoracic wall and a diffuse alveolar pattern consistent with pulmonary oedema. The risk of volume overload and development of pulmonary oedema ± pleural effusion following fluid administration is greater in cats compared with dogs. Pay attention to trends in increasing respiratory rates and any change in respiratory effort. Thoracic ultrasound is a useful, quick and non-invasive way of confirming the presence of a pleural effusion. Restraint for radiography should not be performed if the patient is dyspnoeic, since the stress of the procedure could precipitate a respiratory crisis

The best way to avoid volume overload is to ensure that a careful evaluation of the patient is performed initially, as discussed earlier, to identify occult cardiac disease and other risk factors (see Table 1), and this is coupled with frequent monitoring for the development of early signs of volume overload. Signs include an increase in the respiratory rate and effort, pulmonary crackles and serous nasal discharge. The cat should also be repeatedly assessed for unmasking of occult cardiac disease (eg, development of a heart murmur, gallop rhythm or arrhythmia). If the cat is also hypothermic, its vascular response will be abnormal and it is at greater risk of volume overload. In this scenario, more conservative doses of fluid therapy should be given while warming the cat to avoid volume overload.³

The fluid requirements are assessed on the basis of the history and physical examination and the response to fluid therapy. Administering the calculated fluid deficit in small aliquots allows better assessment of the cat’s ability to cope with this fluid load and endpoints of resuscitation can be used (see box on page 183).

Crystalloids are used initially in the treatment of hypovolaemic shock in the cat. Rather than administering the whole shock volume in one amount, the shock volume can be subdivided into, for example, 1/4 or 1/8 of the calculated blood volume. Thus a bolus of 5–10 ml/kg over 10 mins is recommended, with frequent re-evaluation of the cat based on the endpoints discussed on page 183.³⁰ Lactated Ringer’s is generally an appropriate fluid for resuscitation; 0.9% sodium chloride is an alternative. If the cat shows no improvement, a further two boluses (5–10 ml/kg) of crystalloid can be given. If this is also ineffective, a bolus of colloid (eg, 5 ml/kg over 5–10 mins) should be considered. This bolus can be repeated to effect to improve perfusion parameters. In general, the use of a tetra- or pentastarch is preferred to gelatins. If the cat has initially responded to crystalloid therapy but the effect is short-lived, then colloids can be used to prolong the vascular expansion.

Once the endpoints of resuscitation have been met, the cat can be maintained on crystalloids, which might be combined with a constant rate infusion of colloid, depending on the underlying disease. If despite appropriate fluid resuscitation the cat remains hypotensive and hypovolaemic then use of vasopressors should be considered once other causes of hypotension have been excluded (see arterial blood pressure, page 183).

To try to prevent volume overload and pulmonary oedema, once the systolic blood pressure (SBP) (and CVP, if available) have been stable for 1–2 h, fluid infusion rates should be titrated down to maintain systolic blood pressure and circulating blood volume and address dehydration (see box on page 184). If the cat is anaemic, blood transfusion or administration of a haemoglobin-based oxygen carrier may be considered; if the cat has a bleeding disorder or SIRS then plasma may be required.

Monitoring and supportive measures

Record baseline vital parameters and reassess patient frequently

Temperature, pulse, respiratory rate and localisation of any pain should be recorded from the initial assessment. Vital parameters should be reassessed at frequent intervals (every 5–10 mins), in addition to others used as endpoints for resuscitation, in order to evaluate the response to fluid administration and other treatments.

Pay attention to core body temperature

Addressing hypothermia

Concurrent active warming during fluid resuscitation is important if the cat is hypothermic because the vascular response to fluid therapy is blunted until core temperature rises. Failure to address hypothermia will increase the risk of volume overload developing.³ Direct sources of heat should be avoided to prevent peripheral vasodilation. Use of a forced-air warming device (eg, Bair hugger) or an incubator is ideal if available. If heat mats are used, these should be placed under a soft bed and the cat’s body covered. Wrapping the extremities (with bubble wrap or a light bandage such as Soffban) can also help to prevent further losses, although the main source of heat should be directed to the trunk of the cat’s body. IV fluids can be gently warmed (eg, wrapping drip tubing near the patient in a warm wheat-filled heat pack) and care should be taken to minimise the use of surgical spirit and clipping to prevent further losses.

Significant hypothermia can result in altered platelet function and development of coagulopathic tendencies, abnormal cardiac, renal, hepatic and immune function, and an increased risk of cardiac arrest.³⁴

Addressing hyperthermia

Hyperthermia can be due to true fever (eg, infection, neoplasia or tissue trauma), or situations where heat generation is greater than dissipation (eg, seizures or heat stroke). Mild to moderate increases in temperature are rarely fatal and may have a physiological function in patients with true fever. Temperatures >41.6°C (107°F) are associated with a risk of cellular death, organ failure and disseminated intravascular coagulation. Active cooling is only advocated when the rectal temperature is persistently >41°C (106°F) and is discontinued once the temperature approaches 39.4°C (103°F).³⁵ In this situation administration of oxygen, IV fluids and surface cooling are used (clipping fur, applying tepid water to the body and using a fan). In extremis internal cooling can be performed (eg, gastric and rectal lavage with cooled fluids).

Provide supplemental oxygen

While IV catheter placement and the initial assessment are being performed, it is sensible to provide supplemental oxygen using a flow-by technique with a face mask, if tolerated (Figures 5 and 6). If the cat resents this, try using the oxygen tubing or T-piece alone. Flow rates should be set between 1–3 l/min. If the cat is dyspnoeic, a hands-off approach (eg, using an oxygen tent, incubator or partially covered Elizabethan collar) may be necessary. Ideally, oxygen saturation should thereafter be assessed using a pulse oximeter if available; haemoglobin saturation levels <95% are consistent with hypoxaemia and an indication for ongoing supplemental oxygen. A pulse oximeter probe can be applied to the tongue, or across the phalanx or pinna, depending on the cat’s level of consciousness, although readings can be difficult to obtain if the cat is peripherally vasoconstricted (Figure 7).

Figure 5

Flow-by oxygen should be administered while performing the initial assessment and stabilisation of an acutely collapsed cat

Figure 6

Thoracocentesis being performed to stabilise a dyspnoeic collapsed cat. Note the incontinence sheet laid over a soft bed on the table, supplemental oxygen and minimal restraint being used to facilitate this procedure. Reproduced with permission from the BSAVA manual of feline practice: a foundation manual (in press). © BSAVA

Figure 7

Pulse oximetry can be useful to assess the patient for hypoxaemia. Placement of the probe across the pinna or phalangeal pad is often tolerated in sick cats; however, pigmentation, peripheral vasoconstriction and anaemia may interfere with obtaining a reliable reading. This 6-year-old male neutered domestic shorthair cat presented in congestive heart failure and a pulse oximeter reading was obtained by gently folding the pinna over before applying the probe

If the cat will not tolerate use of a pulse oximeter, mucous membrane colour can provide a subjective assessment of oxygen saturation. Arterial blood–gas analysis could be used to provide additional information but is more challenging in cats and is less available in general practice.

Consider analgesic requirements

Mentation, along with heart and respiratory rate, may be affected by pain (Figure 8). If pain is suspected and the cause of collapse is undetermined, a potent rapid-onset and short-acting analgesic agent is recommended. NSAIDs are contraindicated until hypovolaemia has been addressed and both hepatic and renal function have been assessed. Opioids are a good first-line choice;²⁰ eg, methadone 0.1–0.3 mg/kg slow IV or IM, morphine 0.1–0.3 mg/kg IM, buprenorphine 0.01–0.02 mg/kg IV or IM (remember, however, onset of action of buprenorphine is 30 mins and duration of action is 6–8 h), or pethidine 3–5 mg/kg IM.

Figure 8

Manifestations of pain can be subtle in feline patients. This 10-year-old male neutered Siamese was diagnosed with acute severe pancreatitis and eosinophilic enteritis. (a) Note the hunched body position, staring coat, narrowed palpebral fissure and lowered ear position, which are all typical features of pain. (b) The same patient following treatment for acute pancreatitis and enteritis including opioid analgesia (initially methadone, then buprenorphine). The cat now appears more interactive, looking out from his igloo keenly; his eyes are wide open and he has a normal ear position

Special considerations

Sepsis and SIRS

Sepsis and SIRS are important complications in critically ill patients. They can be associated with organ dysfunction, hypoperfusion and hypotension, and may establish a vicious cycle leading to multiple organ failure. In cats, sepsis tends to be associated with hypodynamic circulatory signs; the hyperdynamic phase of septic shock is less commonly seen.^2,36–38 Diffuse abdominal pain has also been described in severe sepsis, even in patients without abdominal disease.² The source of infection or inflammation may not be obvious; clinicians should maintain an index of suspicion in cases of unexplained acute collapse and perform careful evaluation for more occult disease processes (eg, acute pancreatitis). If SIRS/sepsis are recognised and treated earlier then there is a higher chance of success. Morbidity and mortality rise the more established these syndromes become.

Arrhythmias

Arrhythmias are often secondary to a definable cause and, therefore, treatment should be aimed initially at management of any precipitating factors including electrolyte disorders, acidosis, pain, hypoxia, sepsis, organ failure or cardiomyopathy (if present).³⁹ Autonomic imbalance can be associated with critical illness and, in the authors’ experience, increased vagal stimulation (eg, following vomiting, straining to pass urine or faeces, firm bladder palpation) can increase the risk of vagally induced arrhythmias and cardiopulmonary arrest. Proactive treatment with antiemetics, if nausea is likely, is sensible, as is gentle handling of the bladder.

Altered consciousness

If the cat’s consciousness deteriorates, then urgent assessment for hypotension, hypoglycaemia, hypocalcaemia, hepatic encephalopathy, hypoxia, hyperosmolar conditions (eg, diabetic ketoacidosis), electrolyte and acid–base disorders, thiamine deficiency and toxic conditions should be undertaken.⁴⁰

Persistent hypotension

Hypotension can be due to inadequate circulating volume, inappropriate vasodilation and myocardial dysfunction. If a cat remains hypotensive despite adequate fluid resuscitation then an investigation for complicating factors should be performed. As before, consider the possibility of ongoing fluid loss, hypoxia, electrolyte disorders (hypocalcaemia), hypoglycaemia, acid–base disturbances, hypothermia, cardiac dysfunction (cardiomyopathy and/or arrhythmias), pleural space or pericardial disease, sepsis or SIRS, and institute management as appropriate.⁴¹ Careful attention to reassessment of circulating volume, pain control, oxygen supplementation and cardiac function remains important.

Hypertension

Hypertension is less commonly encountered in critically ill cats, unless it is a cause of the collapse (eg, seizures secondary to hypertensive encephalopathy). Pain, anxiety, fear and volume overload may cause elevations in SBP. False elevations may arise with the use of inappropriately small cuffs; the width of the cuff should measure 40% of the circumference of the distal limb or proximal tail.⁴² Examination of the fundus may reveal signs of hypertensive retinopathy (eg, haemorrhage, retinal detachment) if true hypertension exists. Amlodipine is the first-line treatment (0.625 mg per cat PO q24h initially) and is usually effective within 4–6 h. For severe life-threatening hypertension, parenteral drugs (eg, hydralazine) and continuous blood pressure monitoring should be considered.

Effusions

Suspicion of a pleural or abdominal effusion can be quickly confirmed by ultrasound, if available, whereby free fluid appears hypoechoic (black); if ultrasound is not available blind centesis can be performed. Effusions should be sampled and analysed (biochemistry, cytology ± microbial culture). Pleural effusions should be drained for therapeutic purposes if the cat is dyspnoeic, unless the patient has a coagulopathy. It can be helpful to measure fluid and serum glucose and lactate and to compare values; high lactate and low glucose in the fluid is highly suggestive of sepsis.^43,44

Footnotes

Key Points

Funding

The authors received no specific grant from any funding agency in the public, commercial or not-for-profit sectors for the preparation of this article.

Conflict of interest

The authors do not have any potential conflicts of interest to declare.

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