Page 13 - 麻醉与监护论坛2015年第7期
P. 13
Review and CME Lecture
without rebound tenderness. Hemoglobin was 172g/L, 354.7U/L, creatine kinase isoenzyme (CK-MB) at 31.75μg/
white blood cells were 15.21×109/L, platelets were 86×109/ L, magnesium at 0.34mmol/L and normal for the other
L. Clotting function was normal; ALT was 537.3U/L, AST electrolytes. The patient was in a coma after resuscitation,
was 967.2U/L, LDH was 4178.6U/L, albumin was 31.8g/L, given mild hypothermia ice cap to protect brain,
direct bilirubin was 60.3μmol/L, total bilirubin was 159.4 administrated dexamethasone 40mg/d intravenous infusion
μmol/L, urea was 8.63mmol/L, creatinine was 80.2μmol/ and dopamine 8μg/(min•kg) to maintain blood pressure
L. B ultrasound diagnosis was advanced pregnancy of and rectify acidosis, as well as magnesium supplementation.
singleton breech position. Admission diagnosis was 30+4 The CRRT was implemented continuously to maintain
weeks of intrauterine pregnancy with severe preeclampsia negative balance of the fluid due to anuria. Ventricular
and HELLP syndrome (globally, Level I). Cesarean of fibrillation recurred 10.5 hours later, so defibrillation was
emergency was operated under general anesthesia at the immediately implemented for 2 times besides cardiac
day of admission, and the patient was transferred to the massage. Sinus rhythm renewed 34 min later with heart
intensive care unit (ICU) due to anuria, hyperkalemia, rate of 135/min and blood pressure of 126/96 mmHg. Post-
and acute respiratory distress syndrome (ARDS) after the resuscitation the ECG showed that: I, ST segments of AVL,
operation. Physical examination results were heart rate of V1 to V6 leads arched upward, V1 to V4 leads of which
80/min, blood pressure of 161/103 mmHg. Heart and lung presented tombstone-like changes. Ⅱ, Ⅲ, ST segments of
were normal by the examination. Ventilator was given to AVF lead had a low horizontal pressure, as shown in Figure
assist her breathing, as well as continuous renal replacement 1c. The patient regained consciousness three days after the
therapy (CRRT) at her bedside. Every index was reexamined second resuscitation, but the muscle strengths of limbs were
with hemoglobin at 94g/L, white blood cells at 18.55×109/ evaluated as level 0. Neurotrophic drugs and acupuncture
L, neutrophils at 0.909, platelets at 73×109/L; ALT at 150 treatment were administrated to rectify electrolyte
U/L, AST at 104U/L, albumin at 33.8g/L, total bilirubin at disorders. Muscle strengths gradually restored 15d later.
91.5μmol/L, direct bilirubin at 56.3 μmol/L, urea at 10.9 Due to poor respiratory muscle strength, the patient can
mmol/L, creatinine at 124.6μmol/L, creatine kinase at not live without the ventilator, so getting rid of ventilator
362U/L, lactate dehydrogenase at 624U/L, phosphorus at exercises were gradually implemented until 16 days later
0.87mmol/L, magnesium at 0.41mmol/L. EKG is normal. after extubation. Laboratory examinations pointed out
Three days later, the heart rate of the patient suddenly severe clotting dysfunction after resuscitation: D-dimer
rose in CRRT process, and the ECG displayed ventricular was 7.18 μg/mL, the time of activating partial prothrombin
tachycardia with the highest speed of 154/min, then quickly was 63.8s, thrombin time was 45.5s, prothrombin time
dropping to 36/min, blood pressure undetectable as well. was 119.0s, prothrombin activity was 0.06, international
Cardiac massage was initiated immediately. Repeated normalized ratio was 16.66 and fibrinogen was 1.74g/
intravenous injection of 0.5 mg atropine and 1 mg L. There were multiple purpura in the patient’s skin,
epinephrine was given, but no effect. The ECG displayed
ventricular fibrillation, then given defibrillation three times. Figure 1a R waves of V1-3 leads progressed poorly after
After 55 min of CRP, the ECG showed cardiac rhythm resuscitation, and II, III, AVF leads did not significantly changes
transferred to sinus rhythm with heart rate of 169/min, compared with the former.
blood pressure of 165/120mmHg and oxygen saturation of
100%.
The ECG displayed R waves of chest leads progressed
poorly after resuscitation, as shown in Figure 1a; 4 hours
later Q waves appeared in the ECG, as shown in Figure 1b,
suggesting that the evolution of acute anterior myocardial
infarction was underway. Thus, myocardial enzymes were
examined with troponin T at 0.746μg/L, creatine kinase at
Laboratory RanedvieCwlinaincadlCInMvEesLteigcatutiroen 23 FAM 2013 Jan/Feb Vol.20 Issue 1
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