Emergency Care - Related Articles

Luke F. Rump, DVM

A pet that has suddenly collapsed is very scary to most clients, especially if they have just finished talking with you and everything has been going well. You have just vaccinated “Kodiak” for the second or third time. The client asks, “What is happening? What’s going on? What did you do? You killed him!” This is often asked at loud volume and as one long question rather than separate questions and a statement. One likely possibility is anaphylactic shock. Rapid aggressive treatment gives Kodiak the best chance of recovery.

The initial treatment for anaphylactic shock is epinephrine, oxygen and IV fluids followed by short acting glucocorticoids and antihistamines. Other drugs to consider include atropine, albuterol via inhalation, ranitidine, hetastarch and dopamine.

Causes of anaphylaxis include venoms (insects, spiders, lizards, snakes), vaccinations, foods, blood products, drugs (aminophylline, asparaginase, iodinated contrast media, amphotericin B, others), vitamins (vit K, thiamine, folic acid), NSAIDs, anesthetics, parasiticides and physical factors (heat, cold, exercise).

You have successfully treated Kodiak and you have time to sit back and contemplate the last few minutes. So what did happen? Anaphylaxis can be caused by either an anaphylactic or anaphylactoid reaction. Both causes result in the same clinical appearance and are treated the same. Anaphylactic reactions are a Type I, IgE-mediated hypersensitivity reaction with an interaction of antigen and IgE antibody on the surface of sensitized mast cells. Sensitization requires previous exposure to an antigen or hapten. Once sensitized by cross linking of two IgE molecules, the mast cell is activated and histamine and other inflammatory mediators are released.

Anaphylactoid reactions are caused by direct activation of mast cells to release histamine or by activating the complement pathway without IgE. They do not require previous exposure and sensitization. Inflammatory mediators are divided into primary and secondary mediators. Primary mediators include histamine, heparin, tryptase, kallikreins, proteases, proteoglycans, eosinophilic chemotactic factor of anaphylaxis (ECF-A) and neutrophil chemotactic factor of anaphylaxis (NCF-A). Secondary mediators include prostaglandin E2, PG D2, prostacyclin, leukotrienes, thrombaxane A2 and Platelet activating factor. The initial clinical signs seen in anaphylactic shock are different for dogs and cats. The shock organ in the dog is the liver and in the cat it’s the lungs. Clinical signs seen in the dog can include excitement, vomiting, defecation (often diarrhea) progressing to respiratory distress, collapse secondary to hypovolemic shock and death. You can also see wheals, angioedema, pruritus, pale mucus membranes, poor capillary refill time, tachycardia, poor pulse quality, depression, and collapse as well as respiratory distress in the secondary to upper airway obstruction from laryngeal and pharyngeal edema. Cats, on the other hand, initially show signs of respiratory distress, airway obstruction secondary to laryngeal edema, bronchoconstriction and increased mucus production. Other signs seen in cats include severe pruritis, vomiting, diarrhea, depression and death.

The patients that require the most aggressive treatment are the ones that have the most rapid onset and most severe clinical signs after being exposed to an antigen. Clinical signs often occur within seconds to minutes of exposure. Oral exposures generally take longer to show a reaction. Treatment of anaphylactic shock is supportive and symptomatic in nature. Initial treatment should consist of oxygen, IV fluids and IV epinephrine. Dexamethasone SP and diphenhydramine SQ/IM are the drugs I choose next. The pet should be monitored closely (blood pressure, heart rate/rhythm, respiratory rate and effort) for at least eight hours but there can be reoccurrence of signs in some patients up to three days after exposure.

Epinephrine should be given in all severe anaphylactic reactions. Epinephrine is an adrenergic agent that has both alpha and beta activity. It relaxes smooth muscle in the bronchi and the iris, antagonizes the effects of histamine, increases glycogenolysis, and raises blood sugar. If given by rapid IV injection it causes direct stimulation of the heart (increased heart rate and contractility), and increases systolic blood pressure. If given slowly IV, it usually produces a modest rise in systolic pressure and a decrease in diastolic blood pressure. Total peripheral resistance is decreased because of beta effects (Plumb’s Veterinary Drug Handbook, Fifth Edition). If in full anaphylactic shock, epinephrine should be given at a constant rate infusion rather than bolus injections. A constant rate infusion of epinephrine works better as a vasopressor for the heart than bolus injections. Bolus injections may be beneficial for bronchoconstriction and laryngeal edema. Avoid SQ injections. Dose can be doubled and given intratracheally. Dose 0.05mcg/kg/min CRI; 2.5-5 mcg/kg IV; 5-10 mcg/kg IT; 10 mcg/kg IM. Oxygen- flow by, mask or via endotracheal tube if intubated.

IV fluids are used to support vascular volume. Place an IV catheter and start crystalloids +/- add hetastarch or other colloid. Pets will often need higher than normal fluids rates during shock and in the immediate post shock time period. Fluid rates and patient’s fluid needs should be checked frequently. It helps me to actually do the math to figure out the fluid requirements and to measure/estimate ongoing losses. Shock doses of fluids are 90 mls/kg for dog and 60 mls/kg for cat. Shock doses of fluids for select weights in dogs and cats. 10# Chihuhua = 409 mls; 50# Bulldog = 2045mls; 100# Labrador = 4090 mls; 180# Great Dane = 7363 mls; 10# Cat = 272 mls; 15# Cat = 409 mls. This is a lot of fluids if you need to give a full shock dose. I was taught to start with 1/4-1/2 of a shock dose then reassess your patient to decide if they need more fluids and at what rate. Do not blindly give a whole shock dose.

Colloids can help you decrease the dose of crystalloids needed to improve and then maintain blood pressure. Short acting glucocorticoids can reduce capillary permeability and enhance vasoconstriction. Increased blood pressure can result from both the drugs’ vasoconstrictive properties and increased blood volume that may be produced. Glucocorticoids inhibit fibroblast proliferation, macrophage response to migration inhibiting factor, sensitization of lymphocytes and the cellular response to mediators of inflammation. Glucocorticoids stabilize lysosomal membranes. Glucocorticoids can also antagonize the complement cascade and mask the clinical signs of infection. Mast cells are decreased in number and histamine synthesis is suppressed. (Plumb’s Veterinary Drug Handbook, Fifth Edition). The doses for shock can be very high. The dose of dexamethasone SP for shock in Plumb is 4-6 mg/kg IV (Kemppainen 1986) for dogs and 1 mg/kg for cats. I usually use a lower dose for dogs and rarely go above 1 mg/kg slow IV. Rapid IV injection can cause collapse. Diphenhydramine competitively inhibits histamine at H1 receptors. In addition, it also has substantial sedative, anticholinergic, antitussive, and antiemetic effects. I give 1 mg/lb SQ or IM. I do not give diphenhydramine IV. Other medications may be needed and are based on clinical signs shown by the animal. Additional drugs may be needed for cardiac support- epinephrine as a CRI, hetastarch +/- dopamine. Other drugs to consider include atropine for bradycardia, ranitidine as an H2 blocker, albuterol as a bronchodilator.

Are you sure it was anaphylaxis?

Other diseases that can cause similar signs include severe asthma, inhalation of a foreign body (i.e., dog treat), pheochromocytoma, or mastocytosis. Looking in the mouth to check for a foreign body is a quick and easy thing to do. If necessary you can bypass the oropharynx by placing a long catheter in the trachea and hooking it up to oxygen. This may give you enough time to remove the foreign body or perform a tracheostomy. Prevention is the best course of treatment. Pretreatment with diphenhydramine +/- steroids is an option if you have a history of previous reactions.

Steve Lane, Diplomate ACVIM – Neurology/Neurosurgery

Three percent hydrogen peroxide is quite effective in making dogs and cats vomit. This avoids a visit to a local emergency room or the family veterinarian in an immediate crisis. Reported to be safe when used in small amounts, what follows is a case presentation of hydrogen peroxide induced encephalopathy secondary to 3% hydrogen peroxide ingestion to induce vomition.

History

A 9-year-old mixed-breed dog presented for neurologic assessment after experiencing acute collapse following the administration of 3% hydrogen peroxide. One ounce of hydrogen peroxide had been administered to induce vomition after ingestion of chocolate. After vomition was not induced, the oral dosage was repeated 10 minutes later. Following the second dosage, immediate collapse with a non-responsive and nonambulatory status developed. Emergent presentation ensued.

Examination

At the time of presentation a mentally obtunded status was present. Vital signs were normal. The gums and lips were swollen and bright red. Abnormality was limited to the nervous system. Mentation was characterized as depressed poor response to auditory or tactile stimulation. Ability to maintain sternal recumbency was not possible. Cranial assessment revealed an obtunded mentation with central blindness, depressed facial sensation (symmetric) and absent conjugal eye movements. Gag reflex and tongue function were depressed symmetrically. A non-ambulatory status was present with symmetric motor function present in all limbs. If aided, a based wide stance with generalized ataxia and intentional head tremor was evident. Conscious proprioceptive reactions were absent in all limbs. Hopping reactions were present, although depressed in all limbs. Appendicular reflexes were normal. Spinal palpation was normal and non-painful. Based upon the neurologic examination findings, a diffuse encephalopathy was present. Based upon the history, hydrogen peroxide induced encephalopathy was considered as the primary differential, although it has not been previously reported in the veterinary literature.

Figure 1: T2-wighted coronal acquisition. Areas of fluid diffusion alteration are characterized by a fluffy white appearance. Change is restricted to the grey matter regions of the cerebral and cerebellar cortices.

Figure 2 and 3: Transverse T2 and FLAIR-weighted acquisitions. Areas of cortical hyperintense signal are whiter than the surrounding cortex.

Testing

A complete blood cell count, serum chemistry and urinalysis, bile acid assay, and serum lead levels were submitted. All results were normal. Supportive management utilizing LRS with KCL was instituted pending magnetic resonance imaging and cerebrospinal fluid centesis for analysis.

Magnetic resonance imaging was performed on the cranial axis. Pre and post-contrast T1, T2, FLAIR, T1-post-contrast fat sat and T2-gradient echo acquisitions in sagittal, coronal and transverse sequences were performed. Evident on imaging was symmetric, cellular fluid change characterized by hyperintense signal on T2 and FLAIR weighted acquisitions within the cerebral cortex, thalamus, piriform lobes, corpus callosum, and cerebellar cortex. Noted change was restricted to the gray matter of the cerebral and cerebellar cortices and brainstem. Cerebrospinal fluid centesis revealed a clear, colorless spinal fluid with normal cell count and differential. Protein concentrations were normal.

Diagnosis and Outcome

A working diagnosis of hydrogen peroxide induced polioencephalopathy was made. Supportive management was maintained with gradual and continued resolution of the encephalopathy noted over the initial 60 days. Prognosis for complete recovery is felt to be good.

Discussion

Hydrogen peroxide (H2O2) is a very pale blue liquid that appears colorless in dilute solution. Hydrogen peroxide was first isolated in 1818 by Louis Jacques Thénard by reacting barium peroxide with nitric acid. Hydrogen peroxide is a simple chemical compound. It is water with an extra atom of oxygen attached to it, H2O2. Hydrogen peroxide is valuable as an oxidizing agent like ozone, or bleach for example) because it can release that single oxygen atom in the presence of another reactive substance. This reaction is called oxidation or bleaching. Most people use hydrogen peroxide as an antiseptic. It turns out that it is not very good as an antiseptic, but it is not bad for washing cuts and scrapes and the foaming looks cool. The reason why it foams is because blood and cells contain an enzyme called catalase. Since a cut or scrape contains both blood and damaged cells, there is lots of catalase floating around. When the catalase comes in contact with hydrogen peroxide, it turns the hydrogen peroxide (H2O2) into water (H2O) and oxygen gas (O2).

2H2O2 —> 2H2O + O2

Catalase does this extremely efficiently — up to 200,000 reactions per second. The bubbles you see in the foam are pure oxygen bubbles being created by the catalase. Hydrogen peroxide always decomposes (disproportionate) exothermically into water and oxygen gas spontaneously.

Hydrogen peroxide can be toxic if ingested, inhaled, or by contact with the skin or eyes. Ingestion of hydrogen peroxide is an uncommon source of poisoning resulting in morbidity through three main mechanisms: direct caustic injury, oxygen gas formation and lipid peroxidation. Direct cytotoxic injury through lipid peroxidation can induce blistering of the oral and pharyngeal mucosa, laryngospasm and hemorrhagic gastritis. The production of foam in the oropharynx can lead to obstruction of the larynx or pulmonary aspiration. Early aggressive airway management is critical in patients who have ingested and inhaled concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Ingestion of concentrated hydrogen peroxide can result in the generation of substantial volumes of oxygen. In closed body cavities mechanical distension of a hollow viscus (stomach) secondary to oxygen liberation can induce gastric pain and increase the risk of perforation. Gastric decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release the gas.

Following ingestion, hydrogen peroxide undergoes gastric catabolism producing oxygen and water. When the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial cerebral air gas embolism (CAGE) with subsequent brain infarction. Magnetic resonance imaging in this case demonstrated areas of restricted water diffusion and T2 hyper intensities in multiple vascular territories consistent with ischemia due to CAGE. Extensive cerebrocortical diffusion restriction with apparent gyral edema was evident at 3 days following ingestion, particularly in the parieto-occipital and cerebellar grey matter regions, bilateral. The pattern of imaging in this case closely resembles that of reversible posterior leukoencephalopathy in human beings with hydrogen peroxide ingestion and CAGE.

Conclusion

Despite the label indicating that hydrogen peroxide is toxic, it is reported safe to give to dogs to induce vomition since it induces vomiting and therefore does not stay in the body.

The recommended dosing of hydrogen peroxide is one teaspoon (5 ml) per 10 pounds of body weight. Vomiting should occur within 15 to 20 minutes. If no vomiting occurs, it is reported to be safe to repeat the 3% percent hydrogen peroxide dose once. While the use of hydrogen peroxide represents a safe, economical and, at home treatment to induce vomition, sentinel events can occur with life threatening ramifications. This is the first report of dilute (3%) hydrogen peroxide induced encephalopathy in a companion animal.

Luke Rump, DVM (Emergency and Critical Care)

What is it? Why do this?

The Rule of 20 was developed by Dr. Rebecca Kirby to help care for the very sick septic/septic shock patient. It is a list of 20 critical parameters to assess daily to make sure we are treating the animal in the best way possible. It reminds us to look at the whole picture, make sure nothing is overlooked and helps us to evaluate how the patient is responding to our treatment. The goal is to maintain tissue perfusion, detect problems with organ function before organ dysfunction becomes organ failure and to take steps to prevent organ failure. An example of conditions where this is valuable is pancreatitis, parvovirus, peritonitis, sepsis, severe trauma and temperature, central venous pressure and systemic blood pressure. Monitor interstitial volume: mucus membrane, skin turgor, packed cell volume, total solids and serial body weights. Underlying disease and electrolyte abnormalities will determine which fluid choice to make and when to change it during the course of the disease process.

1. Fluid balance

Critically ill/septic animals can have huge fluid losses from the intravascular compartment into third body fluid spaces. Both intravascular and interstitial fluid compartments need to be treated appropriately. Monitor intravascular volume by; mm color, capillary refill time, heart rate, pulse quality, extremity temperature, central venous pressure and systemic blood pressure. Monitor interstitial volume: mucus membrane, skin turgor, packed cell volume, total solids and serial body weights. Underlying disease and electrolyte abnormalities will determine which fluid choice to make and when to change it during the course of the disease process.

2. Oncotic pull/Colloid oncotic pressure

Large molecular weight molecules in the vasculature have the effect of pulling water into the vasculature. Albumin and its associated cations provide approximately 60-70% of the plasma oncotic pressure. Globulin provides the remaining 30-40%. The only way to accurately predict COP is by direct measurement using a colloid osmometer. This is rarely done in the private practice. This leaves us with estimating/guestimating COP using total solids and albumin levels. Inadequate COP contributes to vascular fluid loss and organ and peripheral edema. Peripheral edema occurs later in the disease process than internal organ edema does. Treatment options include hetastarch(HES), fresh frozen plasma (FFP), whole blood and human albumin. Bolus rates of HES 20mls/kg -dog 10-20mls/kg slowly-cats. Maintenance rates of HES- 10- 20mls/kg/day-dog 10-15 mls/kg/day-cat.

3. Albumin

Albumin maintains colloid oncotic pressure (COP), binds endogenous and exogenous substances, mediates coagulation, and is a free radical scavenger. The consequences of hypoalbuminemia include gastrointestinal (GI) dysfunction (delayed gastric emptying, ileus, GI mucosal edema, and enteral feeding intolerance), coagulation effects (hypercoagulability and increased platelet aggregation), oncotic effects, delayed wound healing, interstitial edema, decreased antimicrobial exposure and increased morbidity and mortality. Hypoalbuminemia results in poorer outcomes. Support of serum albumin levels should be part of the treatment goals in all critically ill patients Treat with FFP (fresh frozen plasma), FP (fresh plasma), and human albumin. Human albumin has a very high COP value (> 200mmHg). It has the potential to draw fluids from the interstitial space into the intravascular space. It can be effective at restoring blood volume, increasing total protein, serum albumin and colloid osmotic pressure. Acute complications associated with human albumin administration in dogs included pyrexia, vomiting, coagulopathy, hypertension, tachycardia, and fluid overload. Hypersensitivity reactions can occur both immediate anaphylaxis and delayed immune complex formation. Repeat infusions of human albumin are not recommended. Repeat infusions can induce a potentially fatal, immediate anaphylactic reaction. Human albumin probably should be the colloid of last resort. It is off-label use.

4. Glucose

Glucose is the obligate energy source for the brain. The brain relies on a constant stream of glucose for its energy needs. Hypoglycemia in adult patients should make the clinician suspicious of sepsis. The goal is to achieve a BG between 80 and 140. Supplementation > 5% should be via central vein after placement of a central line catheter.

5. Electrolytes/Acid Base balance— Na, K, Cl, Ca++, Mg

Electrolyte changes are expected in critically ill animals and can have life threatening implications if not dealt with properly.

- Sodium: Is the major determinant of plasma osmolarity. Hypernatremia is common in critically ill animals. Hyper or Hyponatremia can cause CNS signs. Overly rapid correction of either hyper or hyponatremia can cause severe CNS dysfunction.

- Potassium: Normal levels are essential for normal neuromuscular function. Hypokalemia- Clinical signs can be divided into four categories metabolic, neuromuscular, renal and cardiovascular. Tx: in severely hypokalemia animals (K <2.0) may need to supplement up to 80mEq KCl/L. Hyperkalemiaclinical signs: muscle weakness, bradycardia/atrial standstill. Potassium electrolyte abnormalities can be life threatening fairly quickly. Monitor ECG. Hyperkalemia is most commonly seen in urethral obstruction/renal disease. Treatment depends on severity of hyperkalemia. Fluids, 10% calcium gluconate (antagonizes the cardiotoxic effects of hyperK+ but has no effect on serum K concentrations), NaBicarb, 25% dextrose, 25% dextrose with regular insulin, terbutaline.

Calcium—hyperCa+ clinical signs: PU/PD, anorexia, constipation, lethargy and weakness. Severely affected animals can show clinical signs of ataxia, obtundation, listlessness, muscle twitching, seizures, coma and bradycardia. Treatment includes IV fluids, (0.9% saline) diuretics (furosemide), glucocorticoids and calcitonin. Clinical signs in HypoCa++ include muscle tremors/cramping, stiff gait, seizures, panting, and hyperthermia. Treatment options include calcium gluconate, calcitriol, and oral calcium supplementation.

- Magnesium clinical signs: cardiac arrhythmias, neuromuscular signs. Treatment is by supplementing magnesium either IV or orally. Consider treating if patient is not responding to initial treatment for cardiac arrhythmias, hypokalemia and muscle tremors.

6. Oxygenation/ventilation

All tissues need oxygen. Tissue hypoxia can be separated into four types. (1) Hypoxemic hypoxia- due to inadequate arterial oxygenation. Tx with oxygen supplementation. (2) Anemic hypoxia-reduced oxygen carrying capacity of blood either due to decreased Hb or decreased ability of Hb to carry oxygen. (3) Circulatory hypoxia-when capillary circulation is inadequate to meet the tissues oxygen demand. Tx: appropriate fluid support, improved cardiac output. (4) Histotoxic hypoxiafailure of oxygen utilization at the cellular level (cyanide poisoning). Monitor oxygenation/ventilation by evaluating breathing rate/effort, increased inspiratory vs. expiratory effort, obstructive vs restrictive breathing pattern, blood gases, SpO2, end tidal CO2, and lung sounds. You need to check an arterial blood gas to evaluate PaO2. SpO2 measures hemoglobulin saturation. Carbon dioxide is an indication of ventilation and pulmonary function. CO2 can be monitored by using an end-tidal carbon dioxide monitor. Treat with oxygen +/- ventilation support. Options include using flow by oxygen, nasal oxygen, oxygen cage, oxygen hood and hand or mechanical ventilation.

7. Level of consciousness/mentation

Changes can indicate neurologic or metabolic derangements. LOC- alert/responsive, obtunded (depressed), stupor/semi-coma (generally unresponsive, except to vigorous/painful stimuli) or coma. Seizures are a sign of abnormal cerebral electrical activity (primary neurologic or metabolic—i.e., hepatic encephalopathy). A change from a higher level of consciousness to a lower level of consciousness is often caused by increased intracranial pressure (ICP). A decrease in gag reflex predisposes patient to aspiration. Check medication doses- especially sedatives. Sudden changes should prompt a evaluation of serum osmolality (especially if receiving parenteral nutrition, blood glucose). Calculated plasma Osm= 2 Na+ (BUN/2.8) + BG/18. Normal dog – 290-310 mOsm; cat – 290-330 mOsm. Monitor by evaluating level of consciousness, motor activity, respiratory patterns (Cheyne-Stokes breathing, central neurogenic hyperventilation, apneusis, irregular or ataxic breathing), pupil size and reactivity,(unilateral mydriatic, unresponsive pupil, bilateral miosis, bilateral, mydriatic, unresponsive pupils) and oculocephalic reflex. Treatment options are divided into general vs. specific treatment. General supportive measures include preventing hypoxia and preventing hypotension. Specific treatment options are directed at maintaining adequate cerebral perfusion pressure, decreasing cerebral venous blood volume, controlling PaCO2, reducing cerebral edema with hyperosmolar fluid therapy( mannitol, hypertonic saline, furosemide, glucocorticoids) and reducing cerebral metabolic rate (sedation with barbituates, anesthesia, hypothermia).

8. Blood pressure

Noninvasive blood pressure is easy to monitor using Doppler or Dynamap. Invasive (direct) blood pressure monitoring is technically more difficult but more accurate, especially in the critically ill animal. Monitor along with careful physical exam and ECG. The goal is to maintain blood pressure above- 90 systolic MAP of 60. Treatment for hypotension include fluids( crystalloids and colloids), oxygen, heat support, pain control and cardiac support (dopamine/dobutamine, epinephrine).I A L V E T S F O R S P E C I A L P E T S

9. Heart rate, rhythm and contractility

Evaluate heart rate with stethoscope and by palpating pulses. Evaluate pulse synchronicity and quality. Potential findings when evaluating pulses are: weak (decreased cardiac output, peripheral vasoconstriction, decreased pulse pressure, thready and bounding (hyperdynamic state or diastolic run-off). Palpate both femoral and dorsal pedal pulses-a palpable dorsal pedal pulse equals an approximate systolic BP > 80. Arrhythmias can be caused by poor perfusion, hypoxia, electrolyte abnormalities, hypercarbia, acidosis, cardiomyopathy and/or exogenous toxins. Treatment is required if arrhythmias are adversely affecting perfusion or are electrically unstable. Treatment of the underlying problem along with oxygen support and anti-arrhythmic drugs may be indicated. Lidocaine, procainamide, mexiletine, quinidine, atenolol, propranolol, sotalol, amiodarone, diltiazem, and digoxin should be considered based on type of arrhythmia. Use caution as all of these medications can be arrthymogenic.

10. Coagulation

Disorders of hemostasis and coagulation are important causes of morbidity and mortality in critically ill patients. Disseminated intravascular coagulation (DIC) represents an acute, generalized widespread activation of coagulation. DIC can be separated into two phase; the early prothrombotic, hypercoagulable state and the later bleeding phase. The early phase of DIC is very difficult to diagnose but is the best time to start treatment. The later phase is difficult to reverse. Later phase clinical signs include petechiation, hematomas, epistaxis, hemarthrosis, melena, hematuria, and excessive bleeding from needle sticks. Treatment for DIC is directed at the underlying cause, if known, FFP (if have depleted hemostatic factors) and anticoagulants including aspirin, clopidogrel, warfarin, unfractionated heparin, and low molecular weight heparin. There is evidence that using heparin in patients with inflammatory disease should be discouraged. i.e. AIHA dogs. Heparin use in patients with minimal inflammatory disease but high risk of venous thromboembolism is justified.

11. RBC/Hb concentration

The oxygen content of arterial blood is dependent on the amount of functional hemoglobin (Hb), the degree of saturation of the hemoglobin, and the amount of dissolved oxygen in the blood. The ideal hematocrit value is between 27-33%. Monitor PCV/Hb. If using oxyglobin, then Hb will need to be measured directly. Treat with pRBC’s, whole blood and oxyglobin, if you can find it.

12. Renal Function

Monitoring renal function is mandatory in the critical patient. Start with the initial BUN/creat and urine Specific gravity. Renal values and urine output should be monitored during hospitalization. Normal urine output in a well perfused, normally hydrated patient is 1-2 mls/kg/hr. This is ideally monitored using a urinary catheter with a closed collection system. Monitor urinalysis and urine sediment at least daily for signs of infection, renal tubular casts and glucosuria. Treatment options include fluid therapy, diuretics (mannitol/furosemide/dextrose), dopamine, diltiazem and maintaining normal acid-base and electrolyte balance.

13. Immune status, Abx selection/dosages, WBC count

Severe bacterial infections are a common cause of ICU admission. It is best to choose antibiotics based on culture/sensitivity and source/site of the infection. It is important to provide antibiotic coverage for anaerobic infections as well. Monitor CBC, temperature, globulin levels and culture/sensitivity.

14. GI motility/mucosal integrity

Ileus predisposes patient to vomiting and ulceration. Monitor gut sounds, stool production, vomiting and albumin levels. Recumbent patient are at risk of aspiration pneumonia. Anti-emetics to consider include metoclopramide, chlorpromazine, prochlorpromazine, ondansetron, granisetron, dolaestron and maropitant. GI protectants to consider include cimetidine, ranitidine, famotidine, nizatidine, omeprazole, esomeprazole, lansoprazole, apntoprazole, misoprostil and sucralfate.

15. Drug doses and metabolism

Most of our critical patients end up on multiple drugs. Drug doses and possible drug interactions need to be checked and considered. The benefits and risks should be assessed when you are deciding about adding additional medications. The underlying disease/complications (renal, liver) may require an adjustment in dose or dosing interval of medications.

16. Nutrition

Patients can rapidly develop a negative energy and protein balance leading to compromised host defenses, loss of muscle strength, visceral organ atrophy and dysfunction, gastrointestinal breakdown, pneumonia, sepsis and death. Nutrition is best dealt with early in the course of disease. Our options include parenteral nutrition and/or enteral (feeding tubes). Feeding the gut is the most effective way to provide nutrition.

17. Pain control

Clincal signs that can indicate pain include mental depression, tachycardia, tachypnea, restlessness, irritable attitude and hypertension. Pain is easier to prevent than to treat. Consider both narcotics and/or anti-inflammatories. If using NSAIDS you need to insure the kidneys are working and being supported appropriately.

18. Nursing care/patient mobilization

Catheters should be checked daily, be clearly marked as to when placed and what fluids are running in them. Feeding tubes need to be clearly marked and any enteral feeding solutions should be colored with food coloring. Proper warming or cooling measures are used to maintain a normal temperature. Patients should be rotated or kept sternal if recumbent. The patient needs to be kept clean of urine and stool. Physical therapy may also be indicated.

19. Wound care/bandage change

Wounds should be checked daily and changed as indicated. The bandages need to be changed when wet or soiled. Consider outlining bruising with a marker to help assess changes.

20. TLC

Use comfortable, dry bedding and gentle handling. Owner visitations can have a large impact on an animal’s recovery. The Rule of 20 helps me treat the critical patients I see. I use the list as a reminder of what to check and think about in all these cases. A monitored variable is useful only if a change is noticed and acted upon in an appropriate manner. I commonly use the i-STAT portable blood gas analyzer to monitor electrolytes, blood glucose and renal values. CBC and chemistry panels are done less frequently depending on the disease process. A trend of change is often more valuable than a specific individual value.