Cancer in cats and dogs can be the cause of a variety of emergency situations. Either before a cancer diagnosis or with complications related to chemotherapy or advancing disease, these patients can find themselves in the emergency room and require critical care before receiving care from the Oncology team. Patients with cancer can find themselves in the ER for a wide variety of reasons including seizures, metabolic derangements, open wounds, hemorrhage, shock, sepsis, and collapse.
As these patients present to the emergency room, initial diagnostics such as blood chemistry, CBC, urinalysis, and FAST scans can point towards a cancer suspicion. Diagnostics commonly performed in these patients include full bloodwork, three view thoracic radiographs, abdominal ultrasound, CT or MRI advanced imaging, and bone marrow aspiration. Fine needle aspirates and fluid cytology can also be performed in-house in an attempt to guide treatment. Immediate stabilization including pain management, fluid therapy, blood transfusions, and quality of life discussions are commonly carried out in the ER.
Regardless of the cause, hypovolemic shock is the most common presentation for oncology patients in the ER. Blood and fluid loss can occur from tumors bleeding into the peritoneal or thoracic cavity, through vomiting and diarrhea after chemotherapy, or shock can result from decreased intake due to disease. The cause of shock in small animal patients is the product of a deficit of oxygen supply and oxygen demand. When a lack of oxygen delivery from poor perfusion occurs, cells cannot produce necessary energy. Every cell in the body requires ATP to protect cell wall integrity and perform cellular functions. ATP has a life span of 3 seconds, and the body needs oxygen to create ATP and keep up with need. In a shock situation, because the body is no longer able to provide normal blood flow to tissues oxygen distribution is interrupted, ATP production decreases, and cells begin to die.
The body has baroreceptors to warn the body of decreased blood flow in an attempt to avoid this cell death. These receptors are located in the aorta and kidneys and in times of hypovolemia (for example) sense when blood flow is low and signal back to the body that blood flow is lacking. The sympathetic nervous system reacts with vasoconstriction, increased cardiac contractility, and tachycardia. These adjustments will increase cardiac output in an attempt to maintain blood flow and oxygen flow as normal. The kidneys, via the renin-angiotensin- aldosterone system, will begin to retain sodium and water to increase intravascular volume. These compensatory efforts will display as subtle clinical signs of early shock and are often missed by pet owners.
As shock progresses without any intervention, these compensatory mechanisms are soon overwhelmed and can no longer keep up the "business as usual" blood flow. Vasoconstriction begins to preferentially decrease blood flow to major organ systems (starting with the periphery, then the gastrointestinal tract, progressing to the liver, then kidneys, and eventually brain) to maintain as much perfusion as possible to the heart, lungs, and brain. This whole body decompensation exhibits in the clinical signs of shock: pale mucous membranes, poor pulse quality, decreased blood pressure, and depressed mentation. If these signs are ignored and treatment not administered, organ systems will fail due to lack of oxygen and the animal will die. Animals can be in shock from either a lack of fluid (dehydration) or a lack of perfusion (hypoperfusion) and in some cases, both. Perfusion and hydration are not the same things, and we can measure these in a patient by using different modalities. Perfusion is monitored by measuring mucous membrane color, capillary refill time, pulse quality, and heart rate. Hydration is monitored by measuring skin turgor, the moisture of mucous membranes, and assessing whether the patient's eyeballs are sunken.
As patients present to the hospital with shock, or as those in the hospital are monitored closely, the nursing team must be aware of and look for the clinical signs of shock. As discussed, the body begins with subtle evidence of compensation that may go unnoticed like light pink mucous membranes, mild mental depression, tachycardia, and mildly prolonged capillary refill time. In compensatory shock, the blood pressure and pulse quality remain normal.
Early decompensated shock sees the patient still trying to keep up with decreased perfusion. Dogs suffering from early decompensated shock will exhibit pale mucous membranes, tachycardia, dull mentation, hypotension, poor pulse quality, and increased capillary refill time. If patients at the beginning of decompensated shock are not assessed and treated, they will continue to worsen. In late decompensated shock the body begins to shut down and can no longer keep up with oxygen needs. The heart rate may be decreased, mm color is white or gray, and pulses may be absent. These patients are minimally responsive or obtunded.
Patients that present with these physiologic signs of shock need immediate treatment. Unless the patient has cardiac disease, the mainstay of shock treatment is intravenous fluid therapy. A large bore short length IV catheter will deliver a significant amount of fluids quickly and should be placed in a cephalic or jugular vein. Crystalloid fluids are electrolyte and water replacement and are administered quickly in an attempt to restore circulating volume and therefore oxygen delivery to cells. The shock dose of crystalloid fluids is 90ml/kg for dogs and 45 to 60ml/kg for cats. This large dose is often divided into smaller amounts (20ml/kg for example) and administered as a quick bolus. Once the bolus is complete, the vital signs are once again assessed. The bolus amount is repeated until vital signs begin to improve. In many cases of hemangiosarcoma, blood products may be required to replace oxygen carrying red blood cells.
It is important to note that cats do not respond to shock the same way dogs do. Cats in shock will often vasodilate (not vasoconstrict like dogs), lose body heat, and often experience extreme hypotension. This hypotension is not necessarily from a low circulating volume. As cats warm back to a normal temperature their vessels will constrict back to normal size. If a lot of fluids are administered to a severely hypothermic cat, the blood pressure may read normal, but as the cat warms vasoconstriction occurs. As their temperature returns to normal the excess fluid from their vascular space can become pulmonary edema. It is important to be judicious with fluid administration on hypothermic cats and focus on warming them as much as providing fluid therapy. While the cat is warming, small (20ml) boluses of crystalloids can be given as they are closely monitored. When their body temperature approaches normal and they are still hypotensive more aggressive IV fluid therapy can begin. Cats can be bradycardic or tachycardic with shock; goals from treatment need to be vital signs approaching normal.
Another common oncologic commonly seen is respiratory distress. Pleural effusion can be the result of multiple diseases and must be treated as soon as possible. If pleural effusion is suspected, thoracocentesis should be performed before radiographs. Fluid can be analyzed in house to grossly identify cellular content, and the patient monitored until the next steps in diagnosis can be made. In some cases, severe lymphadenopathy from lymphoma can impede ventilation and patients present in severe respiratory distress. Pulmonary metastasis will also cause respiratory difficulties and can result in an emergency visit. In the hospital these patients are closely monitored:
Sp02 – results for a patient on supplemental oxygen support should be monitored and show improvement in clinical signs throughout hospitalization. As the patient improves, they should be challenged off of oxygen support for a time and a Sp02 reading taken off oxygen to help wean down to room air. Remember the limitations to Sp02 (ambient light, patient compliance, mucous membrane color)
Respiratory rate and effort – frequent (every 2 hours) monitoring of respiratory rate should be performed. It is important to try and observe the animals in secret as values may change in the presence of a technician. Effort should be noted as well.
Mucous membrane color should be closely monitored; gray or muddy mucous membrane color can mean the patient's respiratory status is worsening.
Heart rate should be closely monitored. Hypoxia will result in tachycardia; evaluate the patient if sudden tachycardia occurs or if the heart rate increases between treatments.
One of the less obvious oncologic emergencies seen is hypercalcemia. Hypercalcemia is commonly caused by elevated parathyroid related protein levels which stimulate osteoclasts to break down bone thereby releasing calcium into the bloodstream, known as bone resorption. Another cause of hypercalcemia is due to calcitriol. Calcitriol, a product of vitamin D metabolism, will lead to increased gastrointestinal absorption and will increase calcium release from bones. Lymphoma is the most common cancer that can cause hypercalcemia, but apocrine gland adenocarcinoma, multiple myeloma, and patients with single tumors can also suffer from increased calcium. The clinical signs of hypercalcemia are nonspecific and easily associated with chemotherapy side effects or mild gastrointestinal upset and can be readily dismissed by owners.
As blood calcium levels rise, animals will commonly experience polyuria and polydipsia, anorexia, vomiting, diarrhea, and lethargy. As blood calcium levels continue to rise, patients will begin to experience kidney impairment and progress to arrhythmias. When measuring blood calcium levels, total calcium and ionized calcium can be measured, depending on the hospital's laboratory abilities. Total calcium is measuring that bound to albumin as well as ionized calcium – that which is biologically available. Patients with hypoalbuminemia may have increased ionized calcium due to decreased protein binding.
Once the diagnosis of hypercalcemia is made, there are a variety of treatments implemented to lower levels. The most important priority in these patients should be volume replacement. Losses from polyuria and decrease intake can leave them clinically dehydrated, and if kidney changes have occurred the animal may not be adequately concentrating urine leading to more loss. Fluid replacement should happen with 0.9% NaCl and not a balanced electrolyte solution. Sodium uses the same cellular pumps as calcium, and by increasing the amount of sodium in circulation, calcium will be excreted at a higher rate. As fluid therapy continues, these patients will need their potassium levels monitored to ensure hypokalemia does not occur.
Once the animal is hydrated, furosemide is often utilized to promote calcium excretion, as with furosemide treatment calcium uptake will not take place in the Loop of Henle. Because furosemide can cause dehydration and kidney impairment due to volume loss, it is important to monitor the patient for hypovolemia and dehydration and not utilize this drug until the patient is hydrated before starting treatment. A 5mg/kg bolus can be administered followed by a CRI at 5mg/kg/hr. Glucocorticoids such as dexamethasone SP or prednisone can also be utilized to decrease gastrointestinal absorption of calcium, increase kidney excretion of calcium, and reduce bone resorption. Pamidronate will also inhibit osteoclast activity and lower calcium levels but can also deplete magnesium levels and should be used when magnesium monitoring is available. EDTA can be utilized in dire circumstances if the patient is dying from hypercalcemia as it will chelate calcium, but its use can lead to acute kidney injury.
Hypercalcemia and its necessary treatments and risk of kidney damage require close monitoring by the nursing team. Nursing care must be tailored to the patient, as each patient will have a varying severity of disease and response to treatment. Urine output is one of the top monitoring needs and can be evaluated in different ways. Normal urine output is 1–2ml/kg/hr. Once a patient is placed on IV fluids, urine output should approximate fluid input, and 1–2ml/kg/hr while on IV fluids is considered oliguria. Measurement can be obtained by catching urine on walks for dogs, by utilizing plastic cat litter beads and measuring from the litter box in cats, by weighing bedding prior to placing it in the kennel and again after the patient has urinated on it (1gram of weight=1ml of urine), or by placing a urinary catheter. Urinary catheters are often a source of urinary tract infections, so it is important to not only place the catheter using the appropriate aseptic technique but to also care for the catheter throughout the hospital stay. Keep the catheter clean of feces and dirt, change the patient bedding frequently, and every 8 hours wipe the entire catheter and collection set with 0.05% chlorhexidine solution. If the patient allows, flushing the vaginal vault or prepuce with the dilute chlorhexidine should be performed.
Body weight must be measured multiple times per day, at a minimum the patient should be weighed twice daily. Weight gain can signify the body's inability to process fluids and may be the first clue that necessitates fluid rate changes. The same scale should be utilized each weight session to ensure comparable results.
Patients must be monitored closely for signs of edema. Edema below IV catheter tape is common; worse cases may see pitting edema as excess fluid leaks from capillaries. These patients should be monitored for chemosis as well which can signify possible fluid overload. Clear nasal discharge may appear and should be noted. Along those lines, the patient should be ausculted multiple times per day listening for crackles and wheezes signifying pulmonary edema and an inability to handle the IV fluids. Occult cardiac disease in cats can make itself known during IV fluid therapy and will complicate treatment.
Acute Tumor Lysis Syndrome is an uncommon but potentially catastrophic response to chemotherapy. Patients at the most risk for acute tumor lysis are those with abdominal tumors or those with high tumor loads. It can occur the next hours to days post chemotherapy and involves a significant number of tumor cells dying and lysing at the same time. These patients will suffer from acute hyperkalemia due to the high concentration of potassium inside cells. Hyperkalemia is a dangerous condition due to potassium's role in cardiac muscle cells. As the potassium concentration is greater inside the cells, this creates a negative charge within the cell causing potassium to quickly leave (as it travels down the concentration gradient) the cell leading to muscle cell depolarization and quick contraction of the heart muscle. When potassium levels in circulating blood increase to levels above normal, it leaves fewer of the Na+/K- pumps available for use. Fewer available pumps create a slower influx of sodium into the cell, more delayed potassium exiting the cell, and slower depolarization of the cardiac cells. Slower depolarization is reflected in ECG tracings with the disappearance of P waves, increased size of T waves, and widening of the QRS complex. Hyperkalemia can be addressed first with intravenous calcium gluconate (10% 0.5–1.5ml/kg IV slowly). Administering calcium gluconate is a major step in treatment although it does not alter the level of circulating potassium. When administered IV, calcium gluconate makes the charge outside of the cardiac cells more positive, thereby stabilizing the cell membrane and correcting ECG abnormalities. While calcium gluconate does not often lead to normal sinus rhythm before relieving the urinary obstruction, it will correct the most dangerous arrhythmias and lead to a better anesthetic candidate. Regular insulin (0.5U/kg IV) and intravenous dextrose are also administered to combat hyperkalemia. As insulin allows for glucose to be utilized intracellularly, it will also force potassium to enter the cell thereby reducing the circulating levels. Dextrose is administered as a bolus IV and then as a CRI until blood glucose levels normalize. Beta-adrenergic agonists like terbutaline (0.01mg/kg slow IV) and albuterol (1–3 puffs from an inhaler) will have the effect of driving potassium intracellularly by increasing sodium and potassium ATPase activity. Lastly, sodium bicarbonate (1–2mEq/kg slow IV) can be administered. As H+ is moved out of cells to decrease the pH after sodium bicarbonate infusion, potassium will be moved intracellularly. In humans, CRI administration has been more successful than a single injection. Patients must be able to ventilate appropriately as sodium bicarbonate is changed into CO2 which the patient needs to be able to remove via the respiratory system.
Oncology patients can be critically ill and medically delicate from the time before their diagnosis and throughout their treatment and success in treating them requires a good relationship between the specialties of Oncology and Emergency/Critical Care. Clients need education and information on signs to watch for so that appropriate treatment can be administered. Quality of life and end of life discussions are carried out by both teams and if done properly can make a huge difference in the quality of not only the patient's life but the pet owner as well. While often quite rewarding, working in specialty medicine can also be emotionally challenging. Remember that veterinary teams require quality of work-life discussions and check-ins with each other. By taking care of ourselves, we can continue to provide the best specialty care to our patients.
References available upon request