An 11-year-old, 6.6 kg, female spayed Maltese, presented comatose to the University of Queensland Veterinary Teaching Hospital within 30 minutes of blunt force trauma after being hit by a car. The dog was previously well with no current medications. Initial physical examination revealed the dog to be laterally recumbent and comatose, with bilateral pin-point pupils and an absent menace response. The oral mucous membranes were cyanotic and the dog rapidly progressed to respiratory arrest. The heart rate was initially 60 beats per minute (bpm). Unfortunately, a blood pressure reading was not recorded at this time. There was haemorrhage from the mouth with trauma evident to the oral mucosa.
A venous blood gas performed at presentation showed a mixed acidosis (pH 6.97 [reference interval: 7.35-7.44], lactate 12.4 mmol/L [reference: <2 mmol/L], pCO2 44 mmHg [reference interval: 33.6-41.2 mmHg]), and hyperglycaemia of 24.8 mmol/L [reference interval: 3.3-6.8 mmnol/L]. The sNa was in the normal range at 138 mmol/L [reference interval: 135-153 mmol/L].
An intravenous (IV) catheter was placed and 3 mg alphaxalone was given IV to permit intubation and manual intermittent positive pressure ventilation with 100% oxygen. A 20 ml/kg IV bolus of lactated Ringer's solution (LRS) was administered, followed by a 4 ml/kg bolus of 7% hypertonic saline (HTS) and an infusion of 0.5g/kg of mannitol over 20 minutes. LRS was subsequently continued at approximately 10 ml/kg/hr for one hour and then reduced to 5 ml/kg/hr. Analgesia was provided with fentanyl at 2 ug/kg IV bolus for three sequential boluses, followed by a constant rate infusion (CRI) at 4 ug/kg/hr.
Once spontaneous ventilation was noted, extubation was achieved and treatment continued in an oxygen cage. Neurological status at this time was improving, however, the dog was still obtunded with ongoing bilaterally miotic pupils and an absent menace response. The heart rate had increased to 116 bpm with strong femoral pulses and a systolic blood pressure of 180 mm Hg as measured by doppler. The respiratory rate was 60 breaths per minute with bilaterally harsh lung sounds in all fields. Chest radiographs were performed which demonstrated changes consistent with pulmonary contusions in the right cranial and left caudal lung fields. The dog was assessed as having a TBI with pulmonary contusions.
Approximately two hours after presentation and following initial treatment, a repeat venous blood gas showed the lactate had decreased to near normal at 2.8 mmol/L, with a pH of 7.34, and the hyperglycaemia had resolved (glucose 6.4 mmol/L). The dog's neurological status improved slightly, though some agitation was subsequently noted. A 0.01 mg/kg IV bolus of acepromazine was administered to address this. Five and a half hours after presentation, a venous gas showed a markedly increased sNa of 159 mmol/L (Figure 1). Other blood work remained unremarkable.
The following morning, fourteen hours following presentation the sNa was measured to be 162 mmol/L. A free water deficit of 480 ml was calculated, and her IV fluids were changed to five percent dextrose in water (D5W) at 40 ml/hr, concurrently with LRS at 25 ml/hr. The goal was to replace the free water deficit over 12 to 24 hours with a decrease of sNa of 0.5 mmol/L/hour. Despite this, 24 hours after presentation and 12 hours following free water commencement, the sNa had only decreased by 4 mmol/L to 158 mmol/L. The urine specific gravity (USG) was 1.012 concomitantly (Figure 1).
The dog was noted to have improved consciousness, but was intermittently vocalising. A head tilt to the right and rolling to the left when handled was also noted. The menace response remained bilaterally absent and there was absent conscious proprioception in both forelimbs and delayed in the hindlimbs. Withdrawal was present in all limbs. The dog was noted to be urinating large volumes frequently and refused to eat or drink. Harsh lung sounds were evident bilaterally, with an SpO2 of 94% on room air and 98% whilst receiving cage oxygen. Due to ongoing vocalisation, phenobarbitone at 2 mg/kg slow IV was commenced every 12 hours for sedation.
Approximately forty hours after presentation, the dog's mentation had markedly improved as evidenced by reduced anxiety and vocalisation. The dog was responsive to sound and was able to ambulate with assistance. Oxygen supplementation was discontinued as pulmonary function had normalised, and the fentanyl CRI was reduced to 2 ug/kg/hr. Nutritional support was initiated at this time in the form of Hills a/d slurry via syringe with a total volume of 10 ml given on this day.
Despite ongoing parenteral free water supplementation, the sNa remained elevated at 157 mmol/L, with a USG of 1.005. This poor response to free water supplementation prompted desmopressin (DDAVP) administration, one drop of 4 mug/ml solution into the conjunctival sac. Free water administration continued unaltered. Measurement of sNa 12 hours later revealed no change, remaining steady at 157 mmol/L. Therefore, a second dose of one drop DDAVP was administered conjunctivally. Almost no effect was noted as six hours later; the sNa was 156 mmol/L. At this time the desmopressin dose was increased to two drops every 12 hours. Three hours later, sNa was 151 mmol/L with concurrent D5W at 40 ml/hr and LRS at 25 ml/hr.
The dog's neurological status continued to improve. By the third day the menace response had returned in the left eye; there was reduced rolling and circling, and return of conscious proprioception in both forelimbs was noted. Despite the improvement in neurological status the dog developed intermittent head pressing, displayed ongoing subjective polyuria, and was also noted to be lame in the left foreleg, which continued throughout her hospital stay. A transient increase in rectal temperature was also noted (40.2 C); however, this normalised following active cooling with a fan and was thought most likely secondary to anxiety. Maropitant was administered at 1 mg/kg subcutaneously every 24 hours for suspected nausea (ptyalism) and ongoing inappetence. The dog subsequently began to eat 20 mls of Hills a/d slurry every four to six hours. Water was offered every four hours. LRS and fentanyl were discontinued, and D5W was increased to 50 ml/hr. She was continued on two drops of DDAVP in the conjunctival sac every 12 hours.
Despite this increase in D5W and DDAVP, during the fourth day the dog's sNa had increased again to 156 mmol/L and DDAVP was subsequently increased to three drops every 12 hours. Urine specific gravity was recorded to be 1.010 at the commencement of day 4. A mild hypokalaemia of 3.3 mmol/L (reference range: 3.4-4.9 mmol/L) was noted and LRS with 40 mmol/L KCl was recommenced at 10 ml/hr and the D5W was reduced to 40mls/hr. Four hours after the increase in DDAVP the sNa dropped to 151 mmol/L.
By the fifth day the sNa was between 151 and 153 mmol/L and frequent urination continued. The DDAVP was decreased to two drops every 12 hours, and the fluids remained unchanged.
On the sixth day sNa was 148 mmol/L. The dog became more alert and aggressive, which was consistent with her temperament prior to the TBI. She was starting to lick slurry from a bowl in addition to the syringe feeding commenced earlier. Over the following two days, her sNa remained between 148 and 150 mmol/L with a K of 4.4-4.8 mmol/L and a USG of 1.008. The clinical status remained unchanged and treatment was continued with 2 drops of DDAVP every 12 hours, and the D5W was reduced to 10 ml/hr. The USG increased slightly to 1.012 by day 8.
In the morning of day 9, the dog was ambulatory, although bumping into objects. The sNa was 144 mmol/L, and the DDAVP was therefore discontinued. The following day, the sNa was 140 mmol/L with a K of 6.2 mmol/L. The blood pH was 7.21, bicarbonate 11.2 mmol/L, pCO2 28 mm Hg, and base excess -15.2 mmol/L. The urea was 12.40 (reference interval: 3.40-10.80 mmol/L). She was given sodium bicarbonate (8.4%), 10 mmol, diluted in 50 ml of saline IV over three hours. A urine sample collected by cystocentesis showed cocci on sediment exam and amoxicillin clavulanic acid (12.5 mg/kg) was initiated subcutaneously once daily. The sNa for that day was 146 mmol/L and the K dropped to 5.1 mmol/L.
The dog had improved mentation with no head pressing or circling. Although she was ambulatory without ataxia, she would follow walls when walking. Her vision appeared reduced. The USG was 1.022 with a sNa of 148 mmol/L. She was discharged home on day 13 with oral amoxicillin clavulanic acid.
The dog returned two days later for a recheck, at which time her owner reported almost normal mentation. A repeat sNa was 152 mmol/L with a K of 4.8 mmol/L. She had an ongoing lameness of 4/5 in her left foreleg with no distinct foci of pain on palpation of the limb. Her aggressive behaviour limited the musculoskeletal examination.
During a final recheck 10 days later, the owner reported that her personality and behaviour had returned to what they had been before the accident. Given her ongoing left forelimb lameness, she was anaesthetised the following day after a preanaesthetic blood screen, in which her sNa was 143 mmol/L. Radiographs were taken of both forelimbs and showed bilateral severe osteoarthritis of her elbows, with the left being more severe than the right. The persistent lameness was likely from osteoarthritis exacerbated by trauma.