Critical care basics: Parts 1 & 2 (Proceedings)

Critical care includes around-the-clock nursing and support for vital organ function. Although many specific interventions are determined and driven by monitoring findings, universal patient needs to consider include:

1. Maintain hygiene

2. Nutrition and hydration

3. Analgesia and relief of anxiety

4. Thermoregulation

5. Electrolyte homeostasis

6. Glucose control

7. Thromboembolism prophylaxis

8. Cardiovascular support

9. Respiratory support

Hygiene

At a minimum, sick animals need to have their elimination needs met. Many house pet dogs will refuse to soil a cage unless driven beyond their limit. In addition to predisposing to constipation, urine retention, and bladder dysfunction, soiling the cage may be very distressing to the dog and cause it to expend energy on avoidance behaviors. Cats that are intimidated by the hospital environment may be unwilling to use a litter pan that is in plain view; they may benefit from having it hidden behind or within a cardboard box.

Debilitated animals may not be physically able to properly posture to urinate or defecate and may soil themselves and suffer dermatitis. Methods to limit exposure to urine and feces include elevated cage racks, absorbent pads, "stay dry" pads, towels/blankets, and manual expression of the bladder, and indwelling or intermittent catheterization.

Routine grooming – brushing and combing – feels good to both giver and receiver and reinforces positive interactions with caregivers. It also provides an opportunity to carefully inspect the skin for inflammation or injury and screen for ectoparasites.

Nutrition and hydration

Although many questions remain about when and how to best intervene with nutritional support, there is general agreement that at some point starvation becomes detrimental. In contrast to earlier recommendations that serious illness provoked massive increases in caloric needs, most evidence suggests that caloric needs in sick, recumbent animals rarely exceeds 1.25 x basal energy requirements. Enteral feeding is always preferable to intravenous nutrition, and animals with functional GI tracts should be fed orally whenever possible. When that is not possible, nasoesophageal (NE) or gastric PEG tube feedings should be used in animals that are not vomiting. In animals that can not take gastric feeding, jejunostomy tube feeding may be used assuming intestinal motility is adequate. If gastric stasis is present, metoclopramide (0.1-0.2 mg/kg/hour) may be administered as an IV fluid additive, although in our hands this drug is seldom effective. Some animals respond well to IV or gastric (via PEG or NE tube) erythromycin, 2-10 mg/kg).

Debilitated animals with gastric stasis are at risk for vomiting and aspiration injury. These patients require a nasogastric sump or PEG tube to provide constant or intermittent evacuation of the stomach. This not only prevents vomiting but allows accurate quantification of fluid losses and assessment of antacid therapy (by checking the fluid pH with wide-range litmus paper). Nasogastric tubes may be single (e.g., a 12 French red rubber catheter) or double lumen sump tubes (e.g. Arrow™ Nasogastric Sump).

Water balance is frequently abnormal in sick animals. Although many presented in acute illness are dehydrated and hypovolemic, immobile animals with systemic inflammation are generally prone to tissue edema and fluid administration must be closely monitored with frequent body weight measurements, physical examinations, and laboratory evaluation. The most common fluid therapy mistake made in these patients is the use of high-sodium replacement fluids (e.g., LRS, 0.9% saline, Normasol-R™) to provide maintenance water needs. When administered at a rate appropriate for water needs, these fluids provide sodium at a rate equaling 8-16 times maintenance – much more than the animal would consume in its diet. Whereas relatively healthy animals can excrete this sodium load, those prone to edema (heart disease, systemic inflammation, hypoproteinemia, and immobilization) can not and will suffer consequences of impaired oxygen transport in affected tissues.

Analgesia and sedation

Pain is common in critical illness, and these are the patients least capable of demonstrating their pain with compelling behavioral displays. Systemic inflammation lowers the nociceptive threshold and predisposes to generalized hypersensitivity and allodynia. The neuroendocrine stress response to injury can become sufficiently intense so as to be detrimental. Analgesic therapy is not only necessary for relief of psychic distress, but also to reduce this stress response.

Drug therapy is of no value unless used in a clinic environment that emphasizes the importance of recognizing and aggressively treating pain and other stressors. There is no substitute for dedicated and compassionate nursing care. In humans, post surgical or post injury pain is much more distressing to patients made to feel helpless by an indifferent or unsympathetic nursing staff. Although hospitalized dogs and cats may have fewer psychological needs than their human counterparts, there is every reason to believe that meeting those needs is terribly important to the animal who finds itself removed from its family, placed in an unfamiliar environment, and wounded by the people now in control of its life.

Physical and psychological comforting is absolutely essential. Holding the animal with affection, petting, and brushing teach them that you are not going to approach them only to do something that hurts. Keeping them clean and dry, wetting a dry mouth, cleaning and soothing irritated skin, and helping them shift body position are but a few examples of small acts that make a big difference. Giving cats a place to hide (a familiar carrier or a box placed in the cage with them) or distracting dogs by placing them in areas of activity serves species-specific psychological needs. Bringing in blankets, toys and family members from home for visits helps keep them anchored to the idea that their world is still there, awaiting their return.

Because critically ill patients need frequent blood sampling, placement of a central venous catheter is essential to allow painless (and effortless) collection. Pharmacological sedation is often necessary to facilitate sleep, particularly in relatively vigorous patients after surgery or accidental trauma. Useful drugs include combinations of an opioid and acepromazine (0.01-0.05 mg/kg IV as needed) or dexmedetomidine (0.5 – 3 mcg/kg/hour). The goal should be just enough sedation to promote restful REM sleep, not drug-induced coma. Sedation is not sleep, and failure to sleep because of excessive sedation contributes to ICU psychosis in human patients.

Thermoregulation

Well ventilated, cool rooms create a nice work environment for us but can severely tax small animals trying to maintain normal or elevated temperatures while on a cage rack. Unfortunately, we often do not recognize their efforts to maintain temperature unless they have exhausted all responses short of shivering. At a minimum, all patients should have opportunity to lie on warm, soft bedding. Many clinicians inappropriately confuse fever with environmental hyperthermia. Whereas the latter can be life threatening, elevated temperature from fever is rarely so. Fever should be assisted with blankets, warm water circulating blankets, or warm air circulators. We do not attempt to reduce fevers unless the rectal temperature is > 109° F, or > 106° F and rising rapidly. In that case, parenteral administration of carprofen or meloxicam is indicated to lower the hypothalamic thermostat. Forced cooling is avoided at all costs, as this simply forces the animal to divert more energy towards restoring the fever.

Electrolyte homeostasis

The most common electrolyte disturbances encountered in the seriously ill dog or cat include, in roughly descending order of frequency, magnesium depletion/hypomagnesemia, potassium depletion/hypokalemia, and hyponatremia. Other disturbances that are somewhat specific to particular diseases or conditions include hyperphosphatemia (renal failure), hyperkalemia (renal failure, low cardiac output states), hyperchloremic acidosis (usually secondary to GI losses), hypophosphatemia (secondary to insulin therapy), ionized hypocalcemia (sepsis), and hypercalcemia (neoplasia, hypoadrenocorticism). Acid-base disorders are also seen with some frequency, and metabolic acidosis is the most common.

Magnesium and potassium depletion are routinely encountered in animals that have had reduced food intake and a means of increased loss - typically vomiting, diarrhea, or polyuria. Although serum concentrations of either tend to be low in animals with significant depletion, some may have marked depletion with relatively normal serum concentrations. Therefore, the rate of supplementation is determined by evaluation of serum concentration in light of history (acute vs. chronic, inappetance vs. normal intake, pu/pd) and physical signs (weakness, arrhythmias, prolonged Q-T interval). Magnesium therapy is empiric and has been extrapolated from human medicine. A test dose of 30 mg/kg of magnesium sulfate IV over 5-10 minutes is used in animals with arrhythmias, followed by an infusion of 30 mg/kg/day. The rate of potassium administration ranges from a low of 0.05-0.1 mEq/kg/hour (normal maintenance need) to a 'routine' maximum of 0.5 mEq/kg/hr.

Hyponatremia with hypo-osmolality represents water retention. Although some of these animals have a true whole-body sodium deficiency (in other words, they are hypovolemic), most have normal or even elevated total body sodium content and are retaining water secondary to poor cardiovascular performance, systemic inflammation, or as a response to injury. Careful evaluation of body weight, perfusion status, signs of edema, and laboratory measures is necessary to direct treatment.

Hyperchloremic acidosis (sodium - chloride difference < 32 mEq/l) is usually due to gastrointestinal loss of sodium bicarbonate and is generally the only form of non-respiratory acidosis we consider treating with sodium bicarbonate if acidemia is severe.

Hypophosphatemia is primarily a problem in animals treated with insulin for diabetic ketoacidosis (DKA). Animals with DKA that present with low or normal phosphorus concentrations should be supplemented. When treating DKA with a continuous IV infusion of insulin, potassium phosphate (KPO4) is administered as the sole source of potassium at a rate determined by potassium needs. This rate is typically high (0.25 – 0.5 mEq/kg/hour) and provides an adequate infusion of phosphate. Note that this rate is many times higher than the commonly published phosphate dose of 0.03 mmol/kg/hour.

Glucose control

The complications of hypoglycemia are well known, but recently there has been a growing appreciation in human critical care for the harmful effects of hyperglycemia. In fact, a serum glucose > 180 mg/dl in critically ill patients in a general ICU ward is an independent predictor of mortality, and reductions in morbidity and mortality are had by maintaining the blood glucose between 80 and 140 mg/dl. Although the importance of this in dogs and cats is currently unknown, we routinely administer infusions of insulin to seriously ill animals whose blood glucose exceeds 180 mg/dl, beginning at a rate of 0.05 – 0.1 IU regular insulin/kg/hour, administering a 1 IU/ml dilution via a syringe pump.

A good rule of thumb for a loading dose of glucose in hypoglycemia animals is that 0.4 ml of 50% dextrose/kg lean body weight will raise serum glucose by 100 mg/dl. Depending on the cause of hypoglycemia, the response may be very transient and the patient may require immediate institution of a continuous infusion. When added to IV fluid provided at a maintenance rate, we usually begin with a concentration of 5%. Some animals, notably DKA patients on continuous insulin therapy, need concentrations as high as 20% to avoid hypoglycemia. Concentrations > 7.5% must be administered through a central vein to avoid causing phlebitis.

Thromboembolism prophylaxis

Animals with systemic inflammation, immobility, edema, and IV catheters are at risk for coagulopathies including disseminated intravascular coagulation (DIC) and venous thrombosis. Beyond control of underlying cause there is no consensus on anticoagulant therapy to prevent or treat DIC. We routinely use unfractionated heparin at a dose of 300 IU/kg/day as a fluid additive. In our patient population, this dose will not prolong the aPTT in 90% of cases, allowing us to monitor trends in coagulation profiles. Whether this dose favorably affects the microvascular thrombosis that characterizes the syndrome is unknown.

For animals at risk of deep vein thrombosis/pulmonary embolism (DVT/PTE), we use higher doses of anticoagulant. In humans treated with unfractionated heparin, the aPTT must be prolonged by 50% from baseline to protect against this complication. We start with 50-100 IU/kg intravenously, and begin an infusion of 6-900 IU/kg/day as this is the dose required in most healthy animals to create a comparable response. We measure baseline and follow-up aPTT with a bench top analyzer (SCA2000™, Synbiotics), or confirm an anticoagulant effect with thromboelastography. Alternatively, we use the fractionated product dalteparin at a dose of 100 -200 IU/kg BID, as this product is at least equally effective as unfractionated heparin in humans with less need for monitoring and dose adjustments. Animals we consider for DVT/PTE prophylaxis include those with IMHA, systemic inflammatory diseases (e.g., sepsis, pancreatitis), and immobile animals (particularly if they are too large to provide effective physical therapy).

Cardiovascular support

Normal heart rates for sleeping or sedate dogs in our ICU are 40-80 BPM. If the heart rate in a sleeping or sedate dog is trending upwards or exceeds 120 BPM, we embark on investigations into cause and treat wherever possible. In some, heart rates between 120-140 represent a physiologically appropriate and successful response to increase oxygen demands driven by systemic inflammation or the neuroendocrine response to injury (especially after major surgery). Heart rates > 140 BPM in sedate/sleeping dogs universally indicate serious problems and must be investigated and treated aggressively. Occasionally it is due to efforts at thermoregulation (shivering) and responds to warming. Common pathological causes in our patients include hypovolemia, hypoxemia, anemia, low total vascular resistance from severe sepsis/septic shock, pulmonary hypertension (ARDS, PTE), and intestinal ischemia (mesenteric or portal vein thrombosis).

Similar relationships between heart rate and pathology do not exist in cats, and some relatively healthy cats maintain heart rates > 240 BPM over their entire hospitalization. Observation of trends up or down is more useful in this species than relying on absolute values. The most worrisome finding in sick cats is a heart rate that falls below 160 BPM, a finding common to septic shock and heart failure.

True hypovolemia is ruled out (and treated) by observing the response to a fluid challenge with replacement fluid or colloid; 10-20 ml/kg of replacement fluid (5-10 of colloid) administered RAPIDLY (< 3 minutes) will reliably reduce heart rate in hypovolemic animals with compensatory tachycardia. Equivocal responses should be evaluated further by monitoring the response in central venous pressure to repeated challenges. If the response is favorable, it may be repeated until further improvement is not seen. If one was wrong and there is no response, the dose is small enough to not provoke major complications with edema.

Anemic animals should receive blood or packed red blood cells. Symptomatic animals may benefit from raising their PCV all the way to normal (> 35% in dogs, > 28% in cats). Hypoproteinemic animals with tachycardia are treated with 25% human albumin, plasma, fresh frozen plasma, or starch-based colloid depending on their size and the specific therapeutic goals. Dogs with hypotension from septic shock (where by definition the hypotension is not responsive to fluid loading alone) require vasopressor therapy with norepinephrine (0.2 – 2 mcg/kg/minute) and/or vasopressin (1-4 micro units/kg/minute), along with a 'stress response' dose of steroid (0.02 mg/kg/hour dexamethasone sodium phosphate). Cats with septic shock and relative bradycardia are treated with epinephrine (note: epinephrine is probably harmful to dogs in this setting) at 0.2 – 2 mcg/kg/minute, titrated to increase the heart rate to >/= 180 BPM. If the cat does not respond to the high end of this range, IV atropine may be added (0.02 – 0.04 mg/kg).

Ventricular arrhythmias are not treated unless they compromise cardiac function. This is rare in cats, but occurs in dogs with concurrent heart disease (valvular insufficiency, cardiomyopathy), high metabolic demand, or if the arrhythmia paces the heart above 160 BPM. In that case, we ensure that serum electrolytes (especially potassium) are normalized and treat with lidocaine (dogs only) 2 mg/kg IV, repeated at 2-3 minute intervals to a maximum of 4 doses. If the dog responds, we immediately begin an infusion of 1.8 – 5 mg/kg/hour, using the low end of the range if they responded to just 1 loading dose and a higher infusion if it took 2-4 loading doses. If the dog does not respond to lidocaine, we often try magnesium sulfate 30 mg/kg IV over 5 minutes, procainamide </= 15 mg/kg administered to effect over 45 minutes, or oral sotalol 2-4 mg/kg BID.

Respiratory support

Many of our patients have arterial hypoxemia due to primary lung disease and/or compromised function of the thoracic bellows (neuromuscular weakness, breakdown of the costachondral arch, diaphragm weakness or paralysis). Many are older and have reduced baseline lung function or chronic lung disease superimposed on acute illness. Long-term (hours to days) oxygen supplementation is often essential, and is accomplished with either a commercial oxygen cage or nasal oxygen cannula. "Home made" oxygen cages using a Plexiglas cage door rarely provide much oxygen and should not be used! Nasal oxygen administration can be easily accomplished using a 5-8 French cannula inserted to the depth of the nasopharynx by passing the tube ventral to the middle nasal turbinate.