Anesthesia Case of the Month

Erin L. Wendt-Hornickle Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706.

Search for other papers by Erin L. Wendt-Hornickle in
Current site
Google Scholar
Rebecca A. Johnson Department of Surgical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706.

Search for other papers by Rebecca A. Johnson in
Current site
Google Scholar

Click on author name to view affiliation information


An 8-week-old 0.67-kg (1.47-lb) sexually intact male Chihauahua was evaluated at a referring veterinary clinic after being violently shaken by an Akita. At the time of initial evaluation, the dog was moderately obtunded and tetraparetic but was attempting to ambulate. The right dorsal aspect of the cranium had an asymmetric swelling, and a right head tilt was evident. The dog was unable to see, with miotic pupils bilaterally. The dog had mild left exophthalmia with periocular swelling and right ocular strabismus. Mild epistaxis was present, and upper respiratory sounds were louder than normal. The PCV and TP concentration were 27% and 4.0 g/dL, respectively; blood glucose concentration was too high to register on a glucometer. Insulin (1.56 U/kg [0.71 U/lb], IV) was administered. Results of cytologic examination of a fine-needle aspirate of the cranial swelling were consistent with a diagnosis of hematoma. Skull radiography revealed an open fontanelle with possible skull fractures. Initial treatment included dexamethasone (4.7 mg/kg [2.14 mg/lb], IV), lactated Ringer's solution (18.75 mL/kg [9.4 mL/lb], IV), morphine (0.5 mg/kg [0.23 mg/lb], IM), mannitol (0.25 mg/kg [0.11 mg/lb], IV), and diazepam (0.5 mg/kg, IV). Supportive care was continued for 4 days.

Although the dog's neurologic status was initially stable with some periods of slight improvement, a worsening of neurologic signs was observed 5 days after the dog was attacked, and it was referred to the Small Animal Neurology service at the University of Wisconsin for further evaluation. At this time, the dog was stuporous, nonambulatory, tetraparetic, and laterally recumbent and had intermittent vocalization. Rectal temperature was 33.9°C (93.0°F); pulses were strong and synchronous, and pulse rate was 140 beats/min. Heart and lung sounds during auscultation were considered normal; respiratory rate was 40 breaths/min. Results of abdominal palpation were unremarkable. A large swelling was noted on the right dorsal aspect of the cranium, along with fixed, miotic pupils and bilateral mucopurulent nasal discharge. The gag reflex and physiologic nystagmus were absent. Palpebral reflexes were present bilaterally, but there was no response to additional facial stimulation. The clinical signs were consistent with a diffuse intracranial lesion secondary to trauma.

Computed tomography of the skull and brain was performed to assess the large cranial swelling (Figure 1). Anesthesia was not necessary owing to the patient's mentation; however, oxymorphone (0.05 mg/kg [0.023 mg/lb], IM) was given to facilitate patient positioning. Computed tomography revealed a soft tissue lesion dorsal to the frontal, parietal, and right temporal regions of the skull that extended into the right, dorsolateral aspect of the cranial vault. The parietal bones were severely osteolytic near the fontanelle, creating a 1.5 × 3.2-cm defect in the dorsal calvarium. The right temporal bone had a minimally displaced oblique fracture; the left temporal bone had a comminuted fracture with medial displacement into the cranial vault.

Figure 1—
Figure 1—

Sagittal (A) and transverse (B) CT images of an 8-week-old male Chihuahua that was attacked by another dog. Notice the large soft tissue swelling overlying an area of severe osteolysis of the frontal and parietal bones (arrowheads). The osteolysis has resulted in a 1.5 × 3.2-cm defect in the dorsal calvarium in the region of the bregmatic fontanelle. Fractures of the right and left temporal bones are visible (arrows). One of the fracture fragments is displaced into the cranial vault.

Citation: Journal of the American Veterinary Medical Association 239, 2; 10.2460/javma.239.2.194

Given that the most likely differential diagnosis at this time was a cranial abscess, surgery was planned to decompress the brain and explore the mass. An American Society of Anesthesiologists status of IV was assigned on the basis of the dog's physical condition, rapidly worsening signs, and guarded prognosis. Venous blood was collected for evaluation of PCV and TP and electrolyte concentrations; however, because of the small sample obtained, only PCV (18%) and TP concentration (4.6 g/dL) were evaluated.


What considerations and possible complications must be taken into account when formulating an anesthetic management plan for a dog with neurologic trauma? What considerations must be taken into account when anesthetizing a very small pediatric patient, compared with an adult?


Although anesthesia following nervous system trauma or disease is frequently required in practice (eg, laceration repair following vehicle trauma and anesthesia of patients with epilepsy or intracranial disease), several considerations must be taken into account before general anesthesia is induced. Whether the patient has an open or closed brain injury, maintaining cerebral perfusion is of utmost importance in ensuring adequate delivery of oxygen to neural tissues and maintaining normal CNS function. Several factors are important in maintaining cerebral perfusion, all of which impact CBF. The most important factors are autoregulation of CBF, Paco2, Pao2, CMRO2, and CPP. Thus, the anesthetic goals are to maintain a normal systemic blood pressure and, consequently, normal CBF and CPP; to maintain normal Paco2 and Pao2; and to reduce CMRO2.

Anesthesia of younger patients poses its own challenges. Pediatric canine patients are those in the first 12 weeks after birth. They have immature hepatic metabolic pathways and glucose regulation and higher body water content, lower body fat percentage, and lower serum albumin concentration, compared with adult dogs. These confounding factors influence the choice and dosages of anesthetic drugs. In addition, young patients may also be much smaller than adult patients, which may make body temperature regulation and venous access more challenging.

Anesthetic Management and Outcome

Oxymorphone (0.05 mg/kg, IM) was given prior to CT. Owing to the small vasculature, an intraosseous, right femoral catheter was placed prior to CT to facilitate fluid and contrast administration. Poor tissue enhancement was observed following administration of contrast medium; therefore, patency of the intraosseous catheter was in doubt. For this reason, induction of anesthesia via a mask was chosen. Supplemental oxygen (100%; 4 L/min) was delivered via a mask, and after 5 minutes, anesthesia was induced with sevoflurane (3% to 5%). Once sufficient muscle relaxation was achieved, the dog was endotracheally intubated and connected to a nonrebreathing anesthesia system. Following induction of anesthesia, several attempts at placing a peripheral IV catheter were made. Subsequently, a right jugular vein catheter was placed with minimal jugular vein occlusion to avoid increasing ICP. A blood sample was submitted for evaluation of blood glucose concentration, which was within reference limits (138 mg/dL). Midazolam (0.094 mg/kg [0.043 mg/lb], IV) and an infusion of saline (0.9% NaCl) solution (10 mL/kg/h [4.5 mL/lb/h], IV) were administered. Fentanyl (5 μg/kg/h [2.3 μg/lb/h], IV) was started to reduce the required inhalant concentration and any associated cerebral vasodilation. Anesthesia was maintained with sevoflurane (inspired concentration, 2.0% to 2.5%) in oxygen in combination with fentanyl administration IV. Monitoring throughout anesthesia included measurement of esophageal temperature, pulse oximetry, ECG, analysis of inspired and expired gases, and oscillometric, noninvasive measurement of blood pressure. Body temperature was maintained between 35.7° and 36.3°C (96.2° and 97.4°F). The dog maintained a normal sinus rhythm with a heart rate between 110 and 140 beats/min throughout the procedure, and MAP ranged from 59 to 89 mm Hg. After the dog was moved to the surgery suite, it was attached to a rebreathing anesthesia system and mechanically ventilated at a rate of 20 to 30 breaths/min to maintain Petco2 between 30 and 35 mm Hg. Throughout the anesthetic period, the patient's head position was monitored to ensure that the head remained approximately 30° above the body to allow for adequate venous drainage and prevent increases in ICP.

Surgery was performed by a board-certified neurologist. Intraoperatively, a large abscess was discovered that extended extracranially on either side of the skull beneath the muscle layer as well as intracranially between the remaining bone and the dura. There was also evidence of previous hemorrhage. Although most of the abscess was removed, a small portion of the abscess was tightly adhered to the dura and left in place; samples were collected for bacterial culture and antimicrobial susceptibility testing. There was a small area of cerebral herniation from the left cranial vault through an opening in the frontal and parietal bones. The area was lavaged thoroughly with sterile saline solution, and the muscle and skin were closed in a routine manner.

After surgery, administration of sevoflurane was discontinued and the patient was allowed to breathe 100% oxygen. The fentanyl infusion rate was decreased (3 μg/kg/h [1.36 μg/lb/h], IV) to facilitate recovery and prevent dysphoria while still providing sufficient analgesia. The dog was able to maintain a Petco2 between 35 and 45 mm Hg without assisted ventilation and was extubated when it became restless. Positioning was monitored to keep the dog's head elevated 30° in relation to its body to facilitate venous drainage, prevent an increase in ICP, and reduce the possibility for aspiration (laryngeal reflexes were blunted). The dog was transferred to the critical care unit for postoperative care and observation.

Although some reflexes and postural reactions (ie, hopping) returned after surgery, the dog remained obtunded. Because of financial concerns, the dog was discharged for continuation of care by the referring veterinarian 4 days after surgery. Follow-up communication with the referring veterinarian revealed that the dog had been making minor neurologic improvements until it was again attacked by the same dog 1 month after discharge. The dog was euthanized 45 days after discharge because of concerns related to a poor quality of life.


The incidence of CNS abscess formation in dogs is unknown, but CNS abscesses appear to be uncommon and associated with a high mortality rate. In dogs, they have been reported to develop following bite wounds1 and in response to plant foreign bodies.2 Clinical signs associated with CNS abscesses are mainly due to compression of neurologic structures and associated edema and inflammation. Clinical signs depend on lesion location but can include motor, sensory, and visual impairments as well as mentation and physiologic changes. Although anesthetic management in patients with CNS abnormalities can be challenging, the ultimate goal is to maintain cerebral perfusion by controlling the factors that have an effect on CBF: autoregulation, Paco2, Pao2, CMRO2, and CPP.

Cerebral blood flow has a large effect on ICP because ICP is related to intracranial volume. Normally, an intact, bony, noncompliant skull encases the intracranial structures. In this case, the Monro-Kellie hypothesis states that intracranial volume is the sum of brain, CSF, and blood volumes. Given this, any change in the volume of one constituent must be accompanied by a change in the volume of another to keep intracranial volume and therefore ICP static. If CBF increases, total intracranial volume will increase and ICP will also subsequently increase. If ICP continues to increase, herniation of brain tissue from its normal position within the skull may occur. Signs of brain herniation may include an increase in systolic and pulse pressures, bradycardia, and irregular breathing, collectively known as the Cushing response.3 Efforts at preventing and treating high ICP should be aimed at decreasing the volume of the intracranial constituents. This can be achieved with therapeutic interventions such as hyperventilation and administration of mannitol, hypertonic saline solution, corticosteroids, or diuretics. The treatments chosen depend on the patient's underlying disease process.

In healthy, conscious patients, brain autoregulatory mechanisms control CBF despite changes in CPP, as long as systemic pressures are normal. When systemic blood pressure increases, arteries within the brain constrict; when pressure decreases, arteries dilate.4 Unfortunately, as in this case, these mechanisms can be abolished by head trauma, intracranial masses, and anesthesia.4 Thus, blood flow patterns may be altered in dogs with neurologic trauma by the disease process itself.

Cerebral blood flow is rapidly affected by Paco2, which is why Paco2 is often targeted in the treatment of high ICP. For every 1 mm Hg increase in Paco2 greater than the upper reference limit, CBF increases by 1 mL/100 g of brain tissue/min.4 This is mediated by changes in the pH of the CSF surrounding the arterioles. As the pH decreases with hypercapnia, vasodilation and an increase in ICP result. Thus, it is important to maintain normocapnia to mild hypocapnia (ie, a Paco2 of approx 30 to 35 mm Hg) to prevent or treat intracranial vasodilation. Although normocapnia or mild hypocapnia is best achieved through mechanical ventilation, this may be impractical in some situations and assisted ventilation can be used to maintain an acceptable Paco2.

The Pao2 has an effect on CBF as well but only when it is < 50 mm Hg. With this degree of hypoxemia, cerebral vasodilation will occur, increasing CBF and ICP. Although arterial blood gas analysis is the definitive way to measure Pao2, it may not be available. As such, pulse oximetry can be used, with the understanding that recognition of hypoxemia may be delayed in patients receiving 100% oxygen because of the shape of the oxygen-hemoglobin dissociation curve.5

Cerebral perfusion pressure has a large effect on CBF. Cerebral perfusion pressure is the difference between MAP and ICP. In humans, MAP typically ranges from 60 to 160 mm Hg and ICP typically ranges from 5 to 10 mm Hg. Therefore, CPP is 55 to 150 mm Hg.4 Although species differences exist, when ICP increases, MAP must also increase to maintain CPP. Because hypotension is not uncommon during anesthesia, MAP must be monitored vigilantly and hypotension must be treated aggressively.

Drug choices also impact cerebral perfusion. In this case, we chose oxymorphone and fentanyl as opioid analgesics and midazolam, a benzodiazepine, as a sedative and muscle relaxant. Opioids mediate their effects through μ-opioid receptors and are an acceptable choice for premedication and analgesia in patients with neurologic disorders because opioids have minimal direct effects on CBF and ICP.6 Because opioids can cause hypoventilation, assisted or mechanical ventilation during general anesthesia is recommended to prevent increases in ICP secondary to hypercapnia. Prior to general anesthesia, Petco2 can be monitored by inserting a sampling line intranasally and Paco2 can be monitored by performing blood gas analyses. Benzodiazepines act through γ-aminobutyric acid receptors, opening chloride channels and thus inhibiting cellular excitation.7 They also reduce CBF and ICP, making them optimal choices for dogs that potentially have high ICP.8

We chose sevoflurane for anesthetic induction in the dog described in the present report owing to the lack of IV access. However, barbiturates, etomidate, and propofol all tend to decrease CMRO2 by causing CNS depression and are, therefore, good choices.9 The use of ketamine in patients with neurologic abnormalities is controversial. Unlike other injectable anesthetics, ketamine does not reduce ICP and CMRO2 and should be avoided in veterinary patients with neurologic disorders.8 Mask induction of anesthesia has distinct disadvantages, such as the lack of a controlled airway, difficulty controlling anesthetic depth, and inability to scavenge excess inhalant, and would not have been chosen in this dog if IV induction of anesthesia had been possible.

Volatile anesthetics, such as isoflurane and sevoflurane, when used for maintenance anesthesia, minimally affect CBF at concentrations less than the minimum alveolar concentration, which is approximately 2.6% for sevoflurane in dogs.10 When these drugs are administered at concentrations higher than the minimum alveolar concentration, however, the cerebral blood vessels will dilate, causing an increase in CBF and, possibly, an increase in ICP. Interestingly, with concurrent hypocapnia, these changes are minimized, reinforcing the benefits of assisted or mechanical ventilation.11 Thus, it is important to use a balanced or multimodal approach to the anesthetic plan with the use of preoperative or intraoperative sedatives and analgesics that will permit a reduction in the inhalant concentration required for a surgical anesthetic plane but minimally affect the oxygen supply to the CNS.

Young patients offer their own unique anesthetic challenges. Pediatric patients can have immature hepatic metabolism, resulting in prolonged clearance of drugs. They also have higher body water content and lower body fat percentage, resulting in a smaller compartment for drug redistribution.12 In addition, hypoalbuminemia, whether related to the patient's age or history, can result in a greater portion of the drug being in its active, non–protein-bound form.12 Given these factors, doses of injectable drugs generally should be decreased to reduce the risk of overdose. However, uncontrolled pain in young patients, in which the CNS is still developing, can lead to permanent consequences, such as altered pain perception and increased anxiety.13 Opioid analgesics are appropriate analgesics for pediatric patients, but rather than using opioid dosages reported for adult animals, these drug should be given to effect in pediatric patients.13 Nonsteroidal anti-inflammatory analgesics are not recommended for patients < 6 weeks old because of their immature hepatic and renal systems.12 Hypoglycemia may occur in pediatric patients because of their young age and the stress of anesthesia and surgery. Because glucose is essential to cerebral metabolism and mental alertness, concentrations < 60 mg/dL should be treated with glucose supplementation.12 However, glucose concentrations must be tightly controlled because hyperglycemia (ie, glucose concentration > 180 mg/dL) is associated with poorer outcomes in patients with brain injuries.14

Finally, the small size of the dog described in the present report had to be taken into account during anesthetic planning. The high body surface-to-mass ratio made hypothermia a concern. Perioperative hypothermia is associated with reduced enzymatic activity leading to prolonged drug action, prolonged recovery, a reduction in the minimum alveolar concentration, and cardiac arrhythmias.15 Body temperature should be closely monitored, and warming devices should be used as necessary to maintain core body temperature between 36.67° and 37.8°C (98° and 100°F). In addition, a nonrebreathing circuit system should be used if the patient is not mechanically ventilated. Although this type of breathing system requires high oxygen flows to remove carbon dioxide from the system, which may hasten temperature decreases during anesthesia, it also allows rapid changes in the inspired concentration of inhalant and is associated with lower ventilatory resistance work of breathing in small patients.16

Evaluation and treatment of veterinary patients with CNS trauma are challenging from many standpoints. A presumptive diagnosis is typically made on the basis of history, physical and neurologic examination findings, and results of diagnostic imaging. A definitive diagnosis and surgical intervention should be pursued in patients with severe neurologic deficits. Anesthetic management is challenging and complex but can be successful with the use of multimodal techniques.



Cerebral blood flow


Cerebral metabolic requirement for oxygen


Cerebral perfusion pressure


Computed tomography


Intracranial pressure


Mean arterial blood pressure


End-tidal partial pressure of carbon dioxide


Total protein


  • 1.

    Bilderback AL, Faissler D. Surgical management of a canine intracranial abscess due to a bite wound. J Vet Emerg Crit Care 2009; 19: 712.

    • Search Google Scholar
    • Export Citation
  • 2.

    Mateo I, Lorenzo V, Muñoz A, et al. Brainstem abscess due to plant foreign body in a dog. J Vet Intern Med 2007; 21: 535538.

  • 3.

    Fodstad H, Kelly PJ, Buchfelder M. History of the Cushing reflex. Neurosurgery 2006; 59: 11321137.

  • 4.

    Pasternak JJ, Lanier WL Jr. Diseases affecting the brain. In: Hines RL, Marschall KE, eds. Stoelting's anesthesia and co-existing disease. 5th ed. Philadelphia: Elsevier, 2008;199238.

    • Search Google Scholar
    • Export Citation
  • 5.

    Antonini E. History and theory of the oxyhemoglobin dissociation curve. Crit Care Med 1979; 7: 360367.

  • 6.

    Lamont LA, Mathews KA. Opioids, nonsteroidal anti-inflammatories, and analgesic adjuvants. In: Tranquilli WJ, Thurman JC, Grimm KA, eds. Lumb and Jones' veterinary anesthesia and analgesia. 4th ed. Ames, Iowa: Blackwell Publishing, 2007;241272.

    • Search Google Scholar
    • Export Citation
  • 7.

    Lemke KA. Anticholinergics and sedatives. In: Tranquilli WJ, Thurman JC, Grimm KA, eds. Lumb and Jones' veterinary anesthesia and analgesia. 4th ed. Ames, Iowa: Blackwell Publishing, 2007;203240.

    • Search Google Scholar
    • Export Citation
  • 8.

    Harvey RC, Greene SA, Thomas WB. Neurologic disease. In: Tranquilli WJ, Thurman JC, Grimm KA, eds. Lumb and Jones' veterinary anesthesia and analgesia. 4th ed. Ames, Iowa: Black-well Publishing, 2007;903914.

    • Search Google Scholar
    • Export Citation
  • 9.

    Branson K. Injectable and alternative anesthetic techniques. In: Tranquilli WJ, Thurman JC, Grimm KA, eds. Lumb and Jones' veterinary anesthesia and analgesia. 4th ed. Ames, Iowa: Blackwell Publishing, 2007;273299.

    • Search Google Scholar
    • Export Citation
  • 10.

    Steffey EP, Mama KR. Inhalation anesthetics. In: Tranquilli WJ, Thurman JC, Grimm KA, eds. Lumb and Jones' veterinary anesthesia and analgesia. 4th ed. Ames, Iowa: Blackwell Publishing, 2007;355393.

    • Search Google Scholar
    • Export Citation
  • 11.

    Drummond JC, Todd MM. The response of the feline cerebral circulation to PaCO2 during anesthesia with isoflurane and halothane and during sedation with nitrous oxide. Anesthesiology 1985; 62: 268273.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Pettifer GR, Grubb TL. Neonatal and geriatric patients. In: Tranquilli WJ, Thurman JC, Grimm KA, eds. Lumb and Jones' veterinary anesthesia and analgesia. 4th ed. Ames, Iowa: Blackwell Publishing, 2007;985992.

    • Search Google Scholar
    • Export Citation
  • 13.

    Mathews KA. Pain management for the pregnant, lactating and neonatal to pediatric cat and dog. Vet Clin North Am Small Anim Pract 2008; 38: 12911308.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Claassen J, Vu A, Kreiter KT, et al. Effect of acute physiologic derangements on outcome after subarachnoid hemorrhage. Crit Care Med 2004; 32: 3238.

    • Search Google Scholar
    • Export Citation
  • 15.

    Murison P. Prevention and treatment of perioperative hypothermia in animals under 5 kg bodyweight. In Pract 2001; 23: 412418.

  • 16.

    Hartsfield SM. Anesthetic machines and breathing systems. In: Tranquilli WJ, Thurman JC, Grimm KA, eds. Lumb and Jones' veterinary anesthesia and analgesia. 4th ed. Ames, Iowa: Blackwell Publishing, 2007;453494.

    • Search Google Scholar
    • Export Citation
All Time Past Year Past 30 Days
Abstract Views 62 0 0
Full Text Views 798 768 119
PDF Downloads 82 56 6