SAIM Case Report Example
Case Report #1
Kim Zwerenz-Miks
Patient ID: Sophie
Signalment:
Sophie, 6-month-old, FS, Border Collie, 18.2 kg.
Entering Complaint:
Patient was presented for emergency evaluation after acute collapse on October 21, 2006 and subsequent lethargy.
History:
Owner reported that Sophie was quiet in the morning and reluctant to eat. Progressively became more non-responsive. No vomiting or diarrhea noted by owner.
Sophie is current on all vaccines and has no other health issues. There are other dogs in the household and she lives mostly lives outside. She was spayed 9 weeks ago and had an uneventful recovery. She is currently on no medications.
Initial Physical Exam:
Sophie presented comatose, MM white, tacky, HR 180 bpm, cold extremities, temperature 97.50F. Heart difficult to auscult due to muffling of sounds. No evidence of petechiae, bruising or ecchymosis was seen. Corneas and anterior chambers clear. No ocular discharge. Respiratory rate 60-66 breath per minute with decreased lung sounds in all fields. She had increase respiratory effort with abdominal push. Femoral pulses weak, thready and synchronous. Abdomen tense on palpation. No other abnormalities noted on physical exam.
Problem List:
Problem list included coagulopathy, pulmonary infiltrates and gastroenteritis. Prognosis was guarded.
Intervention:
IV cephalic and saphenous catheters were placed; bleeding at both catheter sites was noted. Bolused 500 mL warmed crystalloids. Initiated heat support (Bair Hugger®) and oxygen support via mask at 5 Lpm. Thoracic ultrasound showed massive pleural effusion. Thoracic radiographs showed pulmonary infiltrates. Abdominal radiographs and ultrasound unremarkable. Initial labs: Lactate 11.9 mmol/L, hemoglobin 5 g/dL, PCV 13%, TP 4 g/L, and ACT 214 seconds. Blood gases showed a mixed metabolic and respiratory acidosis. Blood pulled for CBC, chemistry and coagulation panel. 75mg Vitamin K was given subcutaneously.
Two (2) units of FFP bolused. Thoracocentesis performed and 400 mL of blood (PCV 27%, TP 4) removed from thoracic cavity and autotransfused through hemofilter through saphenous catheter. Two (2) additional units of FFP administered at 5mL/kg/hr. One (1) unit of FWB also transfused, unmatched. Diphenhydramine given SQ. No transfusion reaction noted.
Sophie remained dyspneic with a Sp02 of 90% on Fi02 of 60% - 70%. Follow-up ultrasound revealed that hemothorax reformed. Additional 460mL was removed via thoracocentesis and autotransfused through hemofilter at 5mL/kg/hr. Heart rate decreased to 140 bpm. Lactate decreased to 7.7; ACT decreased to 122 seconds. ECG showed regular rhythm. Placed into oxygen cage at Fi02 of 60%. Movement stimulated emesis/regurgitation producing bloody sputum. Dolasetron (0.6mg) given to help prevent vomiting and nausea. Additionally, famotidine (0.5mg/kg) IV was given to block the action of histamine on stomach cells and reduce stomach acid production. Dolasetron is a serotonin receptor antagonist. Its main affect is to reduce the activity of the vagus nerve, which is a nerve that activates the vomiting center in the brain. Sophie continued to vomit/retch blood when stimulated so a metoclopramide CRI was added. Metoclopramide is a dopamine receptor antagonist which is involved in the vomiting reflex. In addition, metoclopramide is also a prokinetic anti-emetic as it increases the rate of gastric emptying and increases peristalsis.
Harsh lung sounds with mild crackles ausculted. Suspected fluid overload, hemorrhage or ARDS. Sophie developed peripheral edema in all limbs, increased skin turgor, clear nasal discharge and chemosis suggesting a fluid overload situation. Lasix (2mg/kg IV) therapy was initiated. Produced 500mL of urine, sp. Gr. 1.020. Urine dip stick showed 3+ blood, pH 7.0.
Sophie remained dyspneic with expiratory effort even with increasing oxygen support (>80%) and PCV of 30%. Normothermic (100.40 F), RR 60 bpm, lactate 1.2mmol/L. PCV dropped (27%) after lasix administration.
Assessment:
Clinical signs (hemothorax) consistent with warfarin toxicity. Elevated lactate suggests severity of ischemic hit to all major organ systems. Continued dyspnea post thoracocentesis suggests alveolar flooding as well. Rule outs include: transfusion-associated circulatory overload vs. transfusion-related acute lung injury vs. hemorrhage from coagulopathy or combination. Substantial improvement in cardiovascular parameters but prognosis remains guarded due to possible reperfusion injuries. PCV may have dropped due lasix administration causing hemoconcentration then further fluid administration causing dilution. However, continued bleeding has not been ruled out.
Plans:
Continue to monitor in oxygen cage at Fi02 50-50% until hemorrhage is reduced. Vitamin K 2.5 mg/kg PO q 12 hours, famotidine 0.5 mg/kg IV q 12 hours, Dolasetron 0.6 mg/kg SQ q 24 hours. Recheck pleural space with ultrasound q 6 hours; recheck ACT and PCV 6 hrs.
Progress:
CBC unremarkable except for decrease RBCs. Chemistry panel showed a slight increase in BUN and phosphorus and a moderate increase in AST. Coagulation panel was not performed due to delay in the opening of the laboratory. Subsequent lab values after blood products and crystalloids showed a decrease and normalizing of the lactate from 7.7 mmol/L to 0.5mmol/L. ACT also improved significantly from an initial 214 seconds to 86 seconds. PCV also improved to 28%. Respiratory acidosis improved significantly with metabolic compensation. She remained slightly hypercapnia.
Sophie became progressively more dyspneic and orthopneic in light of being maintained at a FiO2 of 70-90% suggesting alveolar flooding. SpO2 was 89- 90%, and mucous membranes were cyanotic.
Thoracic radiographs showed severe defused pulmonary infiltrates, alveolar pattern with extensive air bronchogram. Pulmonary infiltrates most likely due to secondary insult such as ARDS, transfusion - associated circulatory overload or transfusion – related acute lung injury rather than continuing hemorrhage. Recheck thoracic ultrasound showed that the pleural effusion was resolving.
Cardiovascular and coagulation parameters improved almost to normal over the course of treatment. Sophie continued to have nausea, hematemesis, melena and hematochezia, possibly due to ingesting of large quantity of blood and/or reperfusion injury.
Outcome:
Even though Sophie’s coagulopathy and subsequent hemorrhage appeared to be resolving, she was not able to overcome the respiratory insult and pulmonary infiltrates worsened. Sophie was euthanized due to her worsening condition and grave prognosis.
On necropsy, the body as a whole showed hemorrhagic diathesis which was demonstrated in all major organs. Symptoms, laboratory values, response to treatment and necropsy results consistent with warfarin exposure. It is still unclear where and how Sophie came in contact with the substance. Warfarin is an antagonist of vitamin K, a necessary element in the syntheses of clotting factors II, VII, IX and X, as well as naturally occurring endogenous anticoagulant proteins. Lack of clotting factors leads to coagulopathy, and resulting hemorrhage.
Kim Zwerenz-Miks
Patient ID: Sophie
Signalment:
Sophie, 6-month-old, FS, Border Collie, 18.2 kg.
Entering Complaint:
Patient was presented for emergency evaluation after acute collapse on October 21, 2006 and subsequent lethargy.
History:
Owner reported that Sophie was quiet in the morning and reluctant to eat. Progressively became more non-responsive. No vomiting or diarrhea noted by owner.
Sophie is current on all vaccines and has no other health issues. There are other dogs in the household and she lives mostly lives outside. She was spayed 9 weeks ago and had an uneventful recovery. She is currently on no medications.
Initial Physical Exam:
Sophie presented comatose, MM white, tacky, HR 180 bpm, cold extremities, temperature 97.50F. Heart difficult to auscult due to muffling of sounds. No evidence of petechiae, bruising or ecchymosis was seen. Corneas and anterior chambers clear. No ocular discharge. Respiratory rate 60-66 breath per minute with decreased lung sounds in all fields. She had increase respiratory effort with abdominal push. Femoral pulses weak, thready and synchronous. Abdomen tense on palpation. No other abnormalities noted on physical exam.
Problem List:
Problem list included coagulopathy, pulmonary infiltrates and gastroenteritis. Prognosis was guarded.
Intervention:
IV cephalic and saphenous catheters were placed; bleeding at both catheter sites was noted. Bolused 500 mL warmed crystalloids. Initiated heat support (Bair Hugger®) and oxygen support via mask at 5 Lpm. Thoracic ultrasound showed massive pleural effusion. Thoracic radiographs showed pulmonary infiltrates. Abdominal radiographs and ultrasound unremarkable. Initial labs: Lactate 11.9 mmol/L, hemoglobin 5 g/dL, PCV 13%, TP 4 g/L, and ACT 214 seconds. Blood gases showed a mixed metabolic and respiratory acidosis. Blood pulled for CBC, chemistry and coagulation panel. 75mg Vitamin K was given subcutaneously.
Two (2) units of FFP bolused. Thoracocentesis performed and 400 mL of blood (PCV 27%, TP 4) removed from thoracic cavity and autotransfused through hemofilter through saphenous catheter. Two (2) additional units of FFP administered at 5mL/kg/hr. One (1) unit of FWB also transfused, unmatched. Diphenhydramine given SQ. No transfusion reaction noted.
Sophie remained dyspneic with a Sp02 of 90% on Fi02 of 60% - 70%. Follow-up ultrasound revealed that hemothorax reformed. Additional 460mL was removed via thoracocentesis and autotransfused through hemofilter at 5mL/kg/hr. Heart rate decreased to 140 bpm. Lactate decreased to 7.7; ACT decreased to 122 seconds. ECG showed regular rhythm. Placed into oxygen cage at Fi02 of 60%. Movement stimulated emesis/regurgitation producing bloody sputum. Dolasetron (0.6mg) given to help prevent vomiting and nausea. Additionally, famotidine (0.5mg/kg) IV was given to block the action of histamine on stomach cells and reduce stomach acid production. Dolasetron is a serotonin receptor antagonist. Its main affect is to reduce the activity of the vagus nerve, which is a nerve that activates the vomiting center in the brain. Sophie continued to vomit/retch blood when stimulated so a metoclopramide CRI was added. Metoclopramide is a dopamine receptor antagonist which is involved in the vomiting reflex. In addition, metoclopramide is also a prokinetic anti-emetic as it increases the rate of gastric emptying and increases peristalsis.
Harsh lung sounds with mild crackles ausculted. Suspected fluid overload, hemorrhage or ARDS. Sophie developed peripheral edema in all limbs, increased skin turgor, clear nasal discharge and chemosis suggesting a fluid overload situation. Lasix (2mg/kg IV) therapy was initiated. Produced 500mL of urine, sp. Gr. 1.020. Urine dip stick showed 3+ blood, pH 7.0.
Sophie remained dyspneic with expiratory effort even with increasing oxygen support (>80%) and PCV of 30%. Normothermic (100.40 F), RR 60 bpm, lactate 1.2mmol/L. PCV dropped (27%) after lasix administration.
Assessment:
Clinical signs (hemothorax) consistent with warfarin toxicity. Elevated lactate suggests severity of ischemic hit to all major organ systems. Continued dyspnea post thoracocentesis suggests alveolar flooding as well. Rule outs include: transfusion-associated circulatory overload vs. transfusion-related acute lung injury vs. hemorrhage from coagulopathy or combination. Substantial improvement in cardiovascular parameters but prognosis remains guarded due to possible reperfusion injuries. PCV may have dropped due lasix administration causing hemoconcentration then further fluid administration causing dilution. However, continued bleeding has not been ruled out.
Plans:
Continue to monitor in oxygen cage at Fi02 50-50% until hemorrhage is reduced. Vitamin K 2.5 mg/kg PO q 12 hours, famotidine 0.5 mg/kg IV q 12 hours, Dolasetron 0.6 mg/kg SQ q 24 hours. Recheck pleural space with ultrasound q 6 hours; recheck ACT and PCV 6 hrs.
Progress:
CBC unremarkable except for decrease RBCs. Chemistry panel showed a slight increase in BUN and phosphorus and a moderate increase in AST. Coagulation panel was not performed due to delay in the opening of the laboratory. Subsequent lab values after blood products and crystalloids showed a decrease and normalizing of the lactate from 7.7 mmol/L to 0.5mmol/L. ACT also improved significantly from an initial 214 seconds to 86 seconds. PCV also improved to 28%. Respiratory acidosis improved significantly with metabolic compensation. She remained slightly hypercapnia.
Sophie became progressively more dyspneic and orthopneic in light of being maintained at a FiO2 of 70-90% suggesting alveolar flooding. SpO2 was 89- 90%, and mucous membranes were cyanotic.
Thoracic radiographs showed severe defused pulmonary infiltrates, alveolar pattern with extensive air bronchogram. Pulmonary infiltrates most likely due to secondary insult such as ARDS, transfusion - associated circulatory overload or transfusion – related acute lung injury rather than continuing hemorrhage. Recheck thoracic ultrasound showed that the pleural effusion was resolving.
Cardiovascular and coagulation parameters improved almost to normal over the course of treatment. Sophie continued to have nausea, hematemesis, melena and hematochezia, possibly due to ingesting of large quantity of blood and/or reperfusion injury.
Outcome:
Even though Sophie’s coagulopathy and subsequent hemorrhage appeared to be resolving, she was not able to overcome the respiratory insult and pulmonary infiltrates worsened. Sophie was euthanized due to her worsening condition and grave prognosis.
On necropsy, the body as a whole showed hemorrhagic diathesis which was demonstrated in all major organs. Symptoms, laboratory values, response to treatment and necropsy results consistent with warfarin exposure. It is still unclear where and how Sophie came in contact with the substance. Warfarin is an antagonist of vitamin K, a necessary element in the syntheses of clotting factors II, VII, IX and X, as well as naturally occurring endogenous anticoagulant proteins. Lack of clotting factors leads to coagulopathy, and resulting hemorrhage.