Objectives
To review the literature in regards to the pathophysiology of acute spinal cord injury, and to describe current concepts in regards to patient assessment, diagnostic, and therapeutic measures with a special emphasis on emergency and critical care considerations.

Etiology
Acute spinal cord injury occurs in 2 phases. The primary injury occurs at the time of initial injury and may include intervertebral disk herniation, vertebral fracture or luxation, penetrating injury, and vascular anomalies such as fibrocartilaginous embolic myelopathy. Secondary injury occurs following primary injury and is multifactorial encompassing numerous biochemical and vascular events that result in progression of injury.

Diagnosis
The diagnosis is based on history and physical examination findings. A neurologic examination should be performed following initial patient assessment and stabilization. Further diagnostics to characterize acute spinal injury include radiographs and advanced imaging modalities such as myelography, computed tomography, or magnetic resonance imaging.

Therapy
Initial treatment should focus on addressing the patient's cardiovascular and respiratory system. Supportive measures to support systemic perfusion are vital to minimizing secondary injury. Specific therapy toward minimizing secondary injury in veterinary medicine remains controversial, especially in regards to the utilization of methylprednisolone. Other therapies are either in need of additional research or have failed to document clinical difference.

Prognosis
The prognosis for acute spinal injury is varied and is dependent upon the presence of concurrent trauma, location, and type of primary injury sustained, and extent of neurologic impairment at the time of initial presentation. The etiology of the underlying trauma is of great importance in determining prognosis and outcome. Loss of deep pain is generally accepted as a poor prognostic indicator; however, even these patients can recover depending on their response to treatment.

Mechanisms of injury and emergency care of acute spinal cord injury in dogs and cats.

Acute liver injury and acute liver failure are syndromes characterized by a rapid loss of functional hepatocytes in a patient with no evidence of pre-existing liver disease. A variety of inciting causes have been identified, including toxic, infectious, neoplastic, and drug-induced causes. This article reviews the pathophysiology and clinical approach to the acute liver injury/acute liver failure patient, with a particular emphasis on the diagnostic evaluation and care in the acute setting.

Acute liver injury and failure.

Objective

To review the human and veterinary literature regarding gastrointestinal (GI) dysmotility disorders in respect to pathogenesis, patient risk factors, and treatment options in critically ill dogs and cats.



Etiology

GI dysmotility is a common sequela of critical illness in people and small animals. The most common GI motility disorders in critically ill people and small animals include esophageal dysmotility, delayed gastric emptying, functional intestinal obstruction (ie, ileus), and colonic motility abnormalities. Medical conditions associated with the highest risk of GI dysmotility include mechanical ventilation, sepsis, shock, trauma, systemic inflammatory response syndrome, and multiple organ failure. The incidence and pathophysiology of GI dysmotility in critically ill small animals is incompletely understood.



Diagnosis

A presumptive diagnosis of GI dysmotility is often made in high-risk patient populations following detection of persistent regurgitation, vomiting, lack of tolerance of enteral nutrition, abdominal pain, and constipation. Definitive diagnosis is established via radioscintigraphy; however, this diagnostic tool is not readily available and is difficult to perform on small animals. Other diagnostic modalities that have been evaluated include abdominal ultrasonography, radiographic contrast, and tracer studies.



Therapy

Therapy is centered at optimizing GI perfusion, enhancement of GI motility, and early enteral nutrition. Pharmacological interventions are instituted to promote gastric emptying and effective intestinal motility and prevention of complications. Promotility agents, including ranitidine/nizatidine, metoclopramide, erythromycin, and cisapride are the mainstays of therapy in small animals.



Prognosis

The development of complications related to GI dysmotility (eg, gastroesophageal reflux and aspiration) have been associated with increased mortality risk. Institution of prophylaxic therapy is recommended in high-risk patients, however, no consensus exists regarding optimal timing of initiating prophylaxic measures, preference of treatment, or duration of therapy. The prognosis for affected small animal patients remains unknown.

Gastrointestinal dysmotility disorders in critically ill dogs and cats.

Background: Malnutrition is a common problem in critically ill dogs and is associated with increased morbidity and mortality in human medicine. Enteral nutrition (EN) delivery methods have been evaluated in humans to determine which is most effective in achieving caloric goals.



Objectives: To compare continuous infusion and intermittent bolus feeding of EN in dogs admitted to a critical care unit.



Animals: Fifty-four dogs admitted to the critical care unit and requiring nutritional support with a nasoenteric feeding tube.



Methods: Prospective randomized clinical trial. Dogs were randomized to receive either continuous infusion (Group C) or intermittent bolus feeding (Group I) of liquid EN. The percentage of prescribed nutrition delivered (PPND) was calculated every 24 hours. Frequencies of gastrointestinal (GI), mechanical, and technical complications were recorded and gastric residual volumes (GRVs) were measured.



Results: PPND was significantly lower in Group C (98.4%) than Group I (100%). There was no significant difference in GI or mechanical complications, although Group C had a significantly higher rate of technical complications. GRVs did not differ significantly between Group C (3.1 mL/kg) and Group I (6.3 mL/kg) and were not correlated with the incidence of vomiting or regurgitation.



Conclusions and Clinical Importance: There was a statistically significant difference in the PPND between continuously and intermittently fed dogs, but this difference is unlikely to be clinically relevant. Critically ill dogs can be successfully supported with either continuous infusion or intermittent bolus feeding of EN with few complications. Increased GRVs may not warrant termination of enteral feeding.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1939-1676.2010.0487.x

Intermittent and continuous enteral nutrition in critically ill dogs: a prospective randomized trial.

Objective
To define acute liver failure (ALF), review the human and veterinary literature, and discuss the etiologies and current concepts in diagnostic and treatment options for ALF in veterinary and human medicine.

Etiology
In veterinary medicine ALF is most commonly caused by hepatotoxin exposure, infectious agents, inflammatory diseases, trauma, and hypoxic injury.

Diagnosis
A patient may be deemed to be in ALF when there is a progression of acute liver injury with no known previous hepatic disease, the development of hepatic encephalopathy of any grade that occurs within 8 weeks after the onset of hyperbilirubinemia (defined as plasma bilirubin >50 μM/L [>2.9 mg/dL]), and the presence of a coagulopathy. Diagnostic testing to more specifically characterize liver dysfunction or pathology is usually required.

Therapy
Supportive care to aid the failing liver and compensate for the lost functions of the liver remains the cornerstone of care of patients with ALF. Advanced therapeutic options such as extracorporeal liver assist devices and transplantation are currently available in human medicine.

Prognosis
The prognosis for ALF depends upon the etiology, the degree of liver damage, and the response to therapy. In veterinary medicine, the prognosis is generally poor.

Acute liver failure in dogs and cats

Objective – To compare continuous to intermittent feeding at delivering prescribed nutrition in hospitalized canine and feline patients.

Design – Retrospective clinical study.

Setting – University teaching hospital.

Animals – Fifty-four cats and 37 dogs.

Measurements and Main Results – Twenty-four-hour periods of prescribed and delivered nutrition (kcal) were recorded, and the percentage of prescribed nutrition delivered (PPND) was calculated. If the patient received nasoenteric feeding for >1 day, then the average PPND per day was calculated. Frequency of gastrointestinal complications (vomiting, diarrhea, and regurgitation) was calculated per patient for each group. The PPND was not significantly different between patients fed continuously (99.0%) and patients fed intermittently (92.9%). Vomiting affected 29% of patients (26/91), diarrhea affected 26% of patients (24/91), and regurgitation affected 5% of patients (5/91). There was no significant difference in incidence of gastrointestinal complications between the patients fed continuously and the patients fed intermittently. There was a significantly higher incidence of diarrhea and regurgitation in dogs than in cats.

Conclusions – PPND was not significantly different for continuous versus intermittent feeding via nasoenteric tubes. Frequencies of gastrointestinal complications were not significantly different between patients fed continuously and patients fed intermittently. Enterally fed dogs had a significantly higher frequency of regurgitation and diarrhea than enterally fed cats. Prospective studies are warranted to investigate causes for these potential inter-species differences.

Continuous versus intermittent delivery of nutrition via nasoenteric feeding tubes in hospitalized canine and feline patients: 91 patients (2002-2007).

Objective – To describe a rare, but potential clinical manifestation of phenazopyridine (PAP) toxicity in a dog.

Case Summary – A 6-year-old spayed female Chihuahua was evaluated for ataxia and dysphagia after ingestion of 200 mg (66 mg/kg) of PAP hydrochloride. The dog was presented to the hospital with shifting leg lameness involving all 4 limbs, which progressed to reluctance to walk and severe diffuse muscle hyperesthesia. Clinical laboratory abnormalities included marked increases in serum alanine aminotransferase, aspartate aminotransferase, creatine kinase, mild increases in alkaline phosphatase, and increased c-Tnl-troponin concentration. Treatment included administration of intravenous fluids, muscle relaxants, pain medications, and hepatoprotectants for 5 days in the hospital, and medical management at home for an additional 5 days. Follow-up examinations performed 1 and 6 months after initial presentation revealed the dog to be clinically healthy with serum biochemical profiles within reference intervals.

New or Unique Information Provided – The purpose of this report is to describe an unusual manifestation of PAP toxicosis in a dog, which has not been previously reported in the literature. A review of the ASPCA Animal Poison Control Center database revealed 347 cases of PAP exposure in dogs during 2000–2009 underscoring the importance of being aware of this toxicity in the dog.

Melissa L. Holahan

Papers

Continuous versus intermittent delivery of nutrition via nasoenteric feeding tubes in hospitalized canine and feline patients: 91 patients (2002-2007).

Intermittent and continuous enteral nutrition in critically ill dogs: a prospective randomized trial.

Presumptive hepatotoxicity and rhabdomyolysis secondary to phenazopyridine toxicity in a dog.