Residents' Abstracts Presented at the WARC, 2001
Babayan | Chatterjee 1, 2, 3 | Gabriel | King | Nemirovsky | Subbiah | Wang | Yang
Cell saver induced coagulopathy in liver transplant
Babayan E, Ayoub T, Shah P, Patel R
Department of Anesthesiology, Keck School of Medicine, University of Southern California, Los Angeles, CA
Introduction:
Intra-operative blood recovery (cell salvage) is a commonly utilized method
of blood conservation during operative procedures involving significant blood loss. The following case report documents
significant coagulopathy following massive auto-transfusion during Liver transplantation.
Case Presentation:
A 54 year old Hispanic male was admitted to the hospital with end stage
liver failure secondary to Hepatitis C and alcoholic liver cirrhosis for a liver transplant. The patient demonstrated
no systemic symptoms other than those commonly associated with liver failure (anemia, anasarca, massive ascitis,
resolved encephalopathy, esophageal varices and hepato-splenomegaly). One day before surgery, 18 L of ascitic fluid
was drained. Pre-operative coagulation profile showed a PT-13.4, PTT-34.6, and Platelets-87,000. Following an uneventful
induction, a radial arterial line, a multiple lumen central line and PA catheter were inserted without complication.
An aminocaproic acid infusion at a rate of 100mg/hr was initiated.
Over the first four hours the patient was given 6 Units of PRBCs, 2 Units of FFP, 1 Unit of platelets and 225 ml
of cell saver blood. Due to multiple antibodies in the patient's blood and limited availability of cross-matched
bank blood, all cell saver blood salvaged was used to replace blood loss. Four hours into the procedure, blood
loss significantly increased and the amount of blood salvaged was turned to us at rate of 225 ml every 10 minutes.
A total of 7.5 L of cell saver blood was transfused back to the patient over a period of 3 hrs.
Nine hours into the procedure, despite administration of multiple coagulation factors, bleeding became uncontrollable.
The family was informed about the situation and the possibility of an inta-operative death. The result of the coagulation
profile was PT/INR-26/2.28, PTT >100, Fibrinogen 55. The ACT was 450 sec. The issue was discussed with the cell
saver technician, and it was determined that heparin had not been completely washed out from cell saver blood due
to time limitations. It was assumed that PTT and ACT were elevated due to heparin systemically trnsfused. The infusion
of cell saver blood was halted. 250 mg of protamine was administered and the ACT results indicated a dramatic decrease
to 142 sec after which the bleeding subsided significantly. Immediately following additional protamine, the bleeding
was controlled, and the next ACT stabilized at 142. The patient survived this operation, but 3 days post-op he
developed a portal vein thrombosis that necrosed transplanted liver. He received another liver transplant 4 days
later and was discharged home 3 weeks after the second procedure.
Discussion:
In most washed autotransfusion systems (cell savers) red blood cells are
separated from the plasma after anticoagulation with heparin. The blood is processed by centrifugation and the
remaining blood cells are washed with saline. The wash cycle typically uses 750-1500 ml saline per 100-250 ml recovered
RBCs.
Characteristics of recovered blood are following 1:
Complications of cell saver blood transfusion include free hemoglobin, decreased coagulation factors, increased
fibrinogen degradation products and resultant coagulopathy. If a patient receives more than 500-1500 ml of cell
saver blood, febrile reactions and episodes of hypotension are likely. Other complications are hemolysis, and increased
amounts of free hemoglobin can lead to renal damage. If cell saver blood is not washed properly there is a possibility
of increase of heparin concentration in the blood. Variability of heparin activity and pharmacodynamic response
are well documented. Various patient-specific factors also affect pharmacodynamic response to heparin. Therefore,
patients exhibit widely different anticoagulant response to the same standard dose of heparin2.
One of functional measures of heparin in the blood is ACT3. The baseline ACT would be a careful measurement but is not routinely performed in liver
transplant surgery.
Another method to determine heparin concentration in the perioperative setting is protamine titration. Assuming
that the heparin-protamine titration curve of an individual patient remains constant throughout the operative period,
it is possible to determinate heparin concentration to allow a more precise estimation of the amount of protamine
required to neutralize the circulating heparin.
There are also protamine sensors e.g. Novel protamine Sensor4 that detect and quantify the concentration of Heparin via titration with protamine. It eliminates
the need for clot formation and can be used in body fluids like cell saver product, urine, hemofiltrate etc.
The differential diagnosis of coagulopathy in patients during liver transplant surgery is extensive5. The half-lives of the liver-derived coagulation
factors are very short, ranging from 4 days for fibrinogen to a few hours for factor VII. The best estimate of
hepatic function is provided by estimation of prothrombine time. In our case laboratory results show much higher
PTT numbers in comparison to PT. That also points to its possibility of coagulopathy in this patient, mostly secondary
to high levels of heparin in the blood opposed to coagulopathy secondary to impaired liver function or insufficient
transfusion of FFP or platelets.
Severe bleeding in our case far exceeds the deficiency of clotting factors, platelet deficiency, platelet function
abnormality or continued surgical bleeding (major arterial or venous bleed). Because Thromboelastogram machine
was nonfunctional, the only other method of determining Disseminated Intravascular Coagulation would be to measure
fibrin-fibrinogen degradation products.
In our case FFP and platelet transfusion ratio and RBC and platelet transfusion ratio seems more than adequate
(PRBC:FFP = 49:39, RBC:Plt = 49:15). The PT/INR (26/2.2) and PTT (>100) at the height of massive bleeding, suggested
that coagulopathy was heparin induced.
Our first suspicion came when the cell saver technician provided 250 ml blood bags faster than "we could hang
them". The ACT of 450 confirmed the fact that the cell saver blood was not washed properly. Therefore, during
massive bleeding washed blood can be transfused that would further complicate coagulopathy. It is important to
insure time and wash the salvaged product completely in order to avoid coagulopathy and further bleeding.
References:
TOTAL HIP OR KNEE ARTHROPLASTY IN PATIENTS
80 YEARS OF AGE AND OLDER
Taposh Chatterjee, M D. Janos Szenohradszky, M D., Ph. D., Earl M Strum,
M D., Rafat Khan, M D., Rajesh Patel, M D., Edward J McPherson, M D., Ronald L. Katz, MD
Departments of Anesthesia and Orthopedic Surgery,* Keck School of Medicine,
University of Southern California; Los Angeles, CA
ABSTRACT:
A retrospective review was undertaken with IRB approval. The analysis 'included
59 patients (71 arthroplasties) 80 years of age or older, who underwent unilateral primary (n=23) or revision (n=8)
total hip arthroplasty (THA) or primary (n=26) or revision (n=14) total knee arthroplasty (TKA) performed by one
surgeon (E.J.M.) between 1993 and 1998. The purpose of this study was to determine the preoperative medical conditions
and their relation to intraoperative and early postoperative medical problems and complications in this rapidly
growing segment of the population.
METHODS:
The hospital charts were reviewed to obtain demographic data, preexisting
medical conditions and drug therapy, surgery and anesthesia wine, mtraoperative estimated blood loss, blood transfusion,
crystalloid infusion, urine output, post-operative complications and hospital stay. The mortality rate was calculated
for only 49 patients, since 10 patients were lost to follow up. Measured values were expressed as mean ±
SEM. All comparisons were performed using one-way ANOVA and impaired t test with Welch correction. Differences
were considered significant at P<0.05.
RESULTS:
The 59 patients (16 males and 43 females) rangedmi age from 80 to 95 years (83.8 0.4 [mean ± SEM]). 75%
were 80 to 85 years old, 20% were 86 to 90 years old, and 5% were 91 to 95 years old. ASA PS grades were II-IV.
Combined general and epidural anesthesia was used in 31 cases. In 32 cases, general anesthesia alone was used;
epidural anesthesia was given in six cases and spm*al anesthesia in two cases. A pulmonary artery catheter was
miserted in 26 cases and a central venous line in 29 cases. A radial artery catheter was used in all but one patient.
Tables I an 2 show demographic data and other variables. Tables 3 and 4 demonstrate the preoperative medical conditions.
Mild early postoperative complications occured in 70% or 100% of patients undergoing primary or revision THA, respectively.
Complications occured in 23% or 7% after primary or revision TKA patients, respectively (Table 5). There were statistically
significant differences in tourniquet times between the primary and revision TKA patients (Fig. 1), in estimated
blood loss between primary and revision TM and TKA patients (Fig. 2), and in hospital stay between primary and
revision THA and TKA patient's groups (Fig. 3). There was no perloperative mortality. 1.7% of patients died within
3 months after surgery, 6.1% died within 4 years, and 8.2% died within 5 years after surgery.
CONCLUSION:
The data of this retrospective study suggest that the TKA or THA is a safe
procedure in patients 80 years or older. It can be performed with relatively low risk. The level of postoperative
complications was much lower than expected considering the numerous co?existing diseases of the patients. These
results may be attributed to the improved perioperative management and postoperative care that they received.
Renal Cell Carcinoma with Caval and Atrial
Thrombus Protruding into Tricuspid Valve
Taposh Chatterjee M.D, D. Thangathurai MD, FCCM, P. Roffey MD, M. Mogos
MD and P. Lumb MB; BS, FCCM
Department of Anesthesiology, Keck School of Medicine, University of Southern
California, Los Angeles, CA 90033
Introduction:
One percent of patients with renal cell carcinoma can have a tumor thrombus growing into the IVC and atrium. Surgical
removal is the treatment of choice, but involves danger of embolization, extensive hemorrhage and hepatorenal dysfunction.
Case Report:
A 42 year old male presented with left renal cell carcinoma and a large
tumor thrombus growing into the 1VC and right atrium with intermittent protrusion through the tricuspid valve.
The patient successfully underwent left radical nephrectomy with thrombectomy under general anesthesia with a minimal
period of cardiopulmonary bypass during cavotomy and atriotomy.
The patient was induced with Propofol and maintained on lsoflurane, air and oxygen with intermittent Fentanyl and
Ketamine boluses. A double lumen tube was used to improve surgical access in the right chest. The patient was monitored
with standard monitoring and arterial line, and two 9 Fr Cordis were used for venous access. A pulmonary catheter
was not used due to the presence of thrombus. A TEE was used to detect intraoperative embolization and movement
of the thrombus.
Surgical access was through a large T?shaped incision through both chest cavities. Both kidneys were mobilized
with dissection of the IVC and porta hepatis. Prior to cavotomy, the aorta and the SVC were cannulated and the
right kidney cooled with ice slush. The patient was placed on CPB for 30 minutes during which time the right renal
vessels, hepatic artery, portal vein and IVC were clamped, and a cavotomy and atriotomy were performed with removal
of the thrombus from above and below. TEE was used constantly to monitor tumor embolization and its complete removal.
Intraoperatively, the patient was placed on a nitroglycerin infusion to increase venous capacitance and maintain
a state of high tissue perfusion. Mannitol and dopamine infusions were used perioperatively for renal protection.
The patient was extubated on postoperative day 2, and suffered no renal or hepatic dysfunction.
Conclusion:
This case highlights the importance of TEE as an intraoperative monitor
to detect early embolization and complete removal of atrial thrombi. In addition, it emphasizes the role of anesthetic
management to prevent hepatic and renal dysfunction in high risk urological procedures.
KETAMINE AND FENTANYL INFUSION FOR ANALGESIA
IS PREFERABLE IN ELDERLY SURGICAL PATIENTS
Taposh Chatterjee MD, M. Mogos MD, P. Roffey MD, D. Thangathurai, MD
Department of Anesthesiology, Keck School of Medicine, University of Southern
California, Los Angeles, CA 90033
Introduction:
With increased longevity and aggressive surgery for malignancy, it is seen
that a larger number of elderly patients are undergoing extensive surgery. Post operative pain control in such
patients is often fraught with dangers such as hypotension, respiratory depression, confusion and further compromise
of organ systems. We evaluated the efficacy of an infusion of ketamine and fentanyl for pain control in such patients.
Methods:
A retrospective analysis of fifty patients, in the age group greater than
70yrs who underwent extensive surgical procedures such as radical cystectomy, radical prostatectomy, whipple procedure,
pelvic exenteration, etc. was undertaken, and the efficacy of an infusion of ketamine and fentanyl for postoperative
pain control was evaluated. Patients were in ASA PS III-IV. Patients were placed on an infusion of ketamine and
fentanyl postoperatively (ketamine 500mg + fentanyl 1250mcg in 250cc of NS) and infused at a rate of 4-10cc/hr
to keep pain score at 2-4/10 on the Visual Analogue Scale. The average infusion rate was 5cc/hr, which translates
to 10 ing and 25mcg of ketamine and fentanyl, respectively, per hour. Patients were monitored as per their acuity;
respiratory rate and pain scores were monitored and the infusion titrated to analgesia.
Observations:
Ketamine and fentanyl infusions are easy to formulate and use and are relatively
inexpensive. Elderly patients achieved good pain control at infusion rates of 37 cc/hr and did not exhibit respiratory
depression or psychomimetic reactions at the above doses. The infusion also did not predispose the patients to
tachy- or bradycardia and maintained hemodynamic stability for tissue perfusion.
The use of ketamine in the infusion promotes NMDA receptor blockade, provides strong analgesia, has a narcotic
sparing effect and most importantly maintains stable hemodynamics. Fentanyl provides analgesia and sedation and
minimizes the possible psychotropic effects of ketamine.
We therefore propose this method of pain control in the fragile elderly patient and also suggest that this method
may be used when conventional pain management services are unavailable.
NITROGLYCERIN FOR CONTROLLED HYPOTENSION
DURING RADICAL PROSTATECTOMY
Maggy Gabriel, MD., Abraham Goldman, MD., Mariana Mogos, MD., Peter Roffey,
MD., Maged Mikhail, MD., Durayaih Thangathurai, MD.
Department of Anesthesiology, Keck School of Medicine, University of Southern
California, Los Angeles, CA 90033
Objective:
Radical prostatectomy has become the standard, curative treatment for prostate
cancer. The presence of rich venous plexuses at the operative site results in bleeding at the neck of the bladder.
Controlled hypotension technique not only helps decrease blood loss, but also provides a clear and bloodless surgical
field. We are reporting our experience with 2457 patients undergoing this procedure at the USC Medical Center.
Methods:
We conducted a retrospective chart review of patients undergoing radical
prostatectomy over the last 15 years at our institution. General anesthesia was induced with either Pentothal or
Propofol, and was maintained with inhalational agents and narcotics. Blood pressure was monitored by cuff as well
as arterial line. 95% of the patients received controlled hypotension to maintain a mean arterial pressure between
65-80 mmHg during prostate dissection. Different hypotensive techniques were used. In 5% of the patients, beta-blockers,
hydralazine and inhalational agents were used. These techniques were more common in earlier patients studied. In
5% an epidural was used. In 80% of the cases nitroglycerin infusion was used. The average length of surgery was
between 3 to 5 hours. Estimated blood loss was between 300-500cc and there were no intraoperative complications.
Discussion:
During prostate surgery most of the blood loss is from the pelvic venous
plexus. Nitroglycerin facilitates decreasing venous as well as arterial blood pressures while maintaining coronary
and cerebral perfusion. At the same institution, Mikhail et al., measured coronary blood flow while using nitroglycerin
and showed an increase in coronary blood flow despite decreased systemic blood pressures. Nitroglycerin also dilates
the pulmonary vascular bed, decreases platelet aggregation, maintains microvascular blood flow and may have a natriuretic
effect.
Conclusion:
Using nitroglycerin is a safe and effective method to decrease blood loss
in patients undergoing radical prostatectomy.
Prevention of Amphotercin B Nephrotoxicity
in the ICU
M King, D Yang, M Mogos, P Roffey, D Thangathurai, WC Shoemaker
Department of Anesthesiology University of Southern California Keck School
of Medicine, Los Angeles, CA 90033
Introduction:
Amphotericin B is the antifungal agent of choice for systemic fungal infections.
The candida species constitutes the most common etiology in the ICU. Amphotericin B administration is associated
with many adverse reactions. These include fever, rigors, chills, anemia, thrombophlebitis, nausea, vomiting, anorexia,
headache, myalgias, arthralgias, bronchospasm, dyspnea, and tachypnea. However, the most significant side effect
is renal toxicity. Over the years, numerous methods have been employed to prevent such toxicity. In our ICU, a
regimen that ensures adequate intravascular volume and the use of intravenous mannitol has proven most beneficial.
Methods:
We retrospectively studied twenty-seven ICU patients who received amphotericin
B for systemic candidiasis. Two hours prior to starting the amphotericin B, adequate hydration was established
by increasing intravenous fluid rate. This was confirmed by adequate urine output (60-100cc/hr) and hemodynamic
parameters (CVP, PAWP). Intravenous mannitol 20% was started at a rate of 50cc/hr one hour prior to the start time
of the amphotericin B. The total daily dose of amphotericin B was infused over a four-hour period. The intravenous
fluids and the mannitol were continued throughout the amphotericin B administration and for an additional hour
after cessation.
Results:
None of these study patients developed signs or symptoms of renal insufficiency. There were no elevations in creatinine
following the amphotericin B therapy. The total dose of mannitol was 60 grams and the urine output during the mannitol
infusion ranged between 100200 cc/hr. The mean amphotericin B dose was 30.4 ± 11.9 mg over 21 ± 7
days. The mean pre?amphotericin B creatinine was 1.5 ± 0.5 mg/dl and the mean post-amphotericin B creatinine
was 1.4 ± 0.5 mg/dl.
Conclusions:
The ICU houses critically ill patients. Many have multi?system dysfunction and often require numerous forms of
cardiovascular and/or respiratory support in addition broad spectrum to antibiotic therapy. Extreme care must be
taken in order to prevent any further iatrogenic organ impairment. Although the exact mechanism of amphothericine
B nephrotoxicity is not well defined; the possible mechanisms of vasoconstriction and tubuloglomerular feedback
impairment appear to be preventable by using aggressive hydration along with mannitol infusion. The clinical manifestations
of renal tubular acidosis, casts in the urine, azotemia, oliguria, and magnesium and potassium wasting were not
seen when these methods were employed. In the hands of an experienced clinician, amphotericin B will remain the
treatment of choice for serious or disseminated fungal infections in the critical care setting.
A COMPARISON OF ANTINOCICEPTIVE EFFECT OF
THE COMBINATION OF SPINAL MORPHINE OR FENTANYL WITH CLONIDINE PLUS CHOLINESTERASE INHIBITOR IN THE RAT
Alexander Nemirovsky, MD.,Ph.D., Yaoping Zhang, MD., Janos Szenohradszky,
MD, Ph.D., Maxim Benbassat, MD, Vladimir Zelman, MD.,Ph.D.
Department of Anesthesiology Research Laboratory, Keck School of Medicine,
University of Southern California; Los Angeles, CA
INTRODUCTION:
In the previous study [1] we investigated the antinociceptive effect produced by a combination of m-opioid agonist
morphine, a2-adrenergic agonist clonidine and cholinesterase inhibitor physostigmine or neostigmine in the rat
"plantar stimulation" test (the radiant heat-evoked hind paw withdrawal test originally described by
Hargreaves K., et al [2]). The results of that study demonstrated that simultaneous administration of morphine
with clonidine plus physostigmine or neostigmine in the threshold doses, which do not produce any notable side
effects, resulted in a profound antinociception. The aim of the present study was to evaluate the magnitude of
antinociceptive effect produced by the combinations of threshold antinociceptive doses of fentanyl, clonidine and
physostigmine or neostigmine and to compare it with morphine.
METHODS:
Experiments were carried out on male Sprague Dawley rats weighing 300-350g. Morphine (1mg) or fentanyl (1mg), clonidine
(1mg) and physostigmine (10mg) or neostigmine (1mg) were administered intrathecally via the catheter implanted
into the subarachnoid space. The specificity of the effect was investigated with intravenous antagonists, naloxone
(1 mg/kg), yohimbine (1 mg/kg), and atropine (1 mg/kg) respectively. The latencies of nociceptive responses of
all animals were measured by means of a "plantar stimulation" test and converted into % Maximal Possible
Effect (%MPE). Comparisons between groups were carried out with a one-way ANOVA, followed by Student-Newman-Keuls
multiple comparison test. P < 0.05 was considered statistically significant.
RESULTS:
Each of the drugs alone was able to produce a slight increase in the latencies of nociceptive response (Fig.1).
The %MPE was 22.3±2.4, 25.5±1.6, 13.7±2.8, 19.0±1.6, and 25.9±2.1 for morphine,
fentanyl, clonidine, physostigmine and neostigmine, respectively (Fig. 2). Simultaneous administration of morphine
or fentanyl with clonidine plus physostigmine or neostigmine resulted in a dramatic increase in the latencies of
nociceptive response (Fig.3), which in most instances reached the cut-off time (15 sec). The duration of the effect
was also significantly increased. The %MPE produced by the three-drug combination of morphine or fentanyl with
clonidine plus physostigmine or neostigmine (Fig.4) were equal to 83.2±7.3, 83.1±5.9, 98.1±1.2
and 82.7±4.3, respectively, and were significantly greater than the effect produced by any of the two-drug
combinations. Morphine or fentanyl combined with clonidine looks like the best combination among the two-drug group
and the effect produced by any group of the three-drug combinations were similar (p<0.05). Specific antagonists
blocked the effect of m-opioids, a2-adrenergic agoinsts and cholinesterase inhibitors respectively. No notable
side effects were observed throughout the experiment.
CONCLUSIONS:
Simultaneous administration of morphine or fentanyl with clonidine plus
physostigmine or neostigmine in the threshold doses, which do not produce any notable side effects, results in
a profound antinociception in rats. The present study might be of a significant clinical value, since it demonstrates
a way of enhancing analgesia without increasing the risk of undesirable side effects.
References
BISPECTRAL INDEX DURING INTRAVENOUS SEDATION
WITH MONITORED ANESTHESIA CARE
Shunmuga Subbiah, MD, Mary M.Joseph, MD, Uttam K. Sinha MD
Department of Anesthesiology, LAC-USC Medical Center, Los Angeles, California
90033, USA
Bispectral Index (BIS) monitoring was utilized to assess level of conscious sedation. A baseline BIS level was
noted in 20 adult patients then intravenous sedation started with Midazolam 1?2 mg, Fentanyl 0.5?2 ug/Kg and propofol
infusion started at a rate of 25?50 ug/Kg/min.The sedation was titrated till the patient was sedated but arousable.
The monitoring included EKG, Blood pressure, EtCO2 and SaO2. Oxygen was administered via face mask or Nasal Cannula.
The types of Surgeries included Thyroplasty, Biopsies or Tumor excision in the head and Neck area. The BIS level
after sedation ranged between 85?90 when patient was sedated and arousable. At the conclusion of Surgery the propofol
infusion was discontinued and the BIS level returned to baseline within 5 minutes.
Reference:
Kissin I,Anesth Analg 2000:1114-7
Massive Intracardiac/Pulmonary Migrating Thromboembolism
and Gastric Variceal Hemorrhage During Orthotopic Liver Transplantation
Angela Wang MD, R. Patel MD
Department of Anesthesiology, Keck School of Medicine, University of Southern California, Los Angeles, CA
OBJECTIVES:
We describe a case of intraoperative massive migrating cardiac and pulmonary thromboembolism resulting in severe
cardiogenic shock during orthotopic liver transplantation (OLT). Discussion is focused on:
1. The decision making process involved in this case management prior to incision was made.
2. The potential association of pulmonary thromboembolism with prior multiple attempts of transjugular intrahepatic
portosystemic shunt (TIPS) procedure and,
3. Intraoperative management of massive gastric variceal hemorrhage.
CASE REPORT:
The patient was a 62 year-old woman, presented with repeated gastric hemorrhages, diagnosed with cryptogenic hepatocirrhosis
one month prior to her OLT. She had severe portal hyperten-sion with gastric varices, refractory ascites and hepatopulmonary
syndrome. She was transferred to our step-down unit for treatment of her third episodes of gastric variceal hemorrhage
in one week and new onset of hepatoencephalopathy.
After three failed lengthy attempts for TIPS procedure. She came to OR for emergency OLT. Her pre-TIPS bilateral
extremities Doppler was negative for venous thrombus. Her preop PT/INR 24.2/2.13, PTT 34 and the platelet count
was 34k. After the placement of a right radial arterial line, general anesthesia was induced with stable vital
signs. Right IJ was easily cannulated with a 9 Fr. introducer sheath. The PA capillary wedge was achieved about
15 cm distal to the initial observation of the PA tracing. Baseline oxygen saturation was 88% on room air and 99%
on ventilator with FiO2 of 64%. Within this time period, BP was 120-130/50-60, CVP 14-15, PAP 27/17, PACWP 15 and
CO 10.5. Baseline ABG, TEG was pending. One hour after GA induction, the blood pressure suddenly decreased to 60/30.
Incremental doses of epinephrine up to 1mg ivp was needed to maintain MAP ~50 mmHg. CVP reading was off scale.
PA transiently decreased to 15/10 then increased to 65/30. HR up from 90's to 120's-140's. O2 sat ~95% - 99%. EKG
showed sinus tachycardia with single focal ectopies (PVC's/ PACs with BBB?). Dysarrhythmia quickly progressed to
multifocal bigemony (PVCs/PACs with BBB?). It was unresponsive to 50mg intravenous lidocaine. Profound hypotension
was unresponsive to immediate volume replacement (PRBC 1U).
Emergency transesophageal echocardiography revealed a large, mobile, polymorphism and low-density mass that was
situated in the superior vena cava and right atrium. The mass was prolaping into and obstructing the right ventricle
inlet. Color Doppler showed mild TR. The right atrium was severely dilated. The right ventricle and left ventricle
was empty and hyperdynamic. TEG was consistent with hypocoagulopathy. Nitroglycerine was initiated with caution
to decrease PVR in conjunction with vasopressor to maintain hemodynamic stability. After about ten minutes the
patient's vital signs was stabilized. Repeat Echo showed the large thrombus had completely disappeared, presumably
into the pulmonary vasculature. Within 30 min PAP was back to 30~40/18-22, CVP 14-16, O2 sat 99%. ABG showed mild
metabolic acidosis. We proceeded with OLT. TEE was replaced with a NG tube on intermittent low-pressure suction.
The patient tolerated IVC clamping with stable vital signs. Fourteen minutes later, her BP was sagging and heart
rate was picking up despite aggressive volume replacement. NG was manipulated. Bright-red blood of ~2L was suctioned
out. A Salem-Blackmore tube was inserted to temponade GI bleeding with success. The gastric balloon was insufflated
with 150 cc air, The Salem-Blackmore tube was placed on traction. The OLT lasted about 15.5 hours. The patient
was extubated on post-op day 5 and walked out of the hospital on postop day 28.
DISCUSSION:
Coagulopathy in advanced cirrhosis is characterized by a delicate balance of hypercoagulation and hyperthrombolysis.
Aggressive treatment with FFP/platelets in conjunction with antifibrinolitic medicines may tip the balance over
to hypercoagulation. If denuded endothelium is present intravascular thrombosis may occur. Post-TIPS pulmonary
embolism has been reported in the literature. Worsening ascites post-TIPS might be the clue for portothrombus formation
in this case. The morphology and the mobility of the clot seems that it have migrated (from portal system?) rather
than a de nova clot in IJ. Fifteen days after the TIPS procedure when intraoperative IJ was placed, traumatic endothelitis
would have healed and thrombus formation was unlikely. This was evidenced by the hypocoagulopathic state indicated
by TEG. It is very important to appreciate that a negative preoperative Doppler only indicates no clot in the extremities.
It does not rule out the presence of thrombus in other parts of the body.
TIPS is a recommended treatment for severe portal hypertension. However, severe complications have been reported
such as pulmonary thromboembolism, high-output CHF and MI. Anesthesiologists will encounter more patient with TIPS
for OLT. We should be aware of the possibility of intrahepatic thrombosis post-TIPS.
Intracardiac thromboembolism resulted in transient cardiogenic shock in our patient. It rapidly progressed to pulmonary
embolism. Although the thrombus was large the resulting pulmonary hypertension and hypoxia was surprisingly mild.
The patient was possibly benefited from multiple factors related to the nature of her disease. The snowy low-density
image of the clot indicated it was relatively immature (coagulopathy) and prone to breakdown.
The patient's dilated pulmonary vasculature allowed the clot to lodge into distal branches of pulmonary artery.
Her relative hyperfibrinolysis state helped to desolve the clot. Lastly our combined pulmonary vasopressor and
vasodilator therapy served as a massager to mechanically breakdown the thrombus. The treatment of choice for PE
would be haperinization, that this patient would not be able to tolerate due to her active GI hemarrhage. The severe
hypotensive episode was a lethal insult to her cirrhotic liver.
Without OLT a rapid worsening of her hepatic function would cost the patient's life. We chose proceed with OLT,
giving the patient the opportunity to receive a functional liver. She subsequently recovered. We have made a right
decision in this case.
Acute Postoperative Adrenal Insufficiency
Following Retroperitoneal Dissection
D Yang, P Roffey, M Mogos, M King, M Gabriel, and D Thangathurai
Department of Anesthesiology, Keck School of Medicine, University of Southern
California, Los Angeles, CA
Acute adrenal insufficiency is a rarely encountered postoperative complication in young patients. These patients
present diagnostic difficulties in the acute phase. We are reporting a patient who presented postoperatively with
hemodynamic instability unresponsive to hydration and pressor infusions. There were minimal electrolyte changes
to aid in the diagnosis.
Case report:
A 31 year-old male with extensive retroperitoneal metastatic disease secondary to testicular carcinoma was scheduled
for a redo left thoracoabdominal retroperitoneal dissection. The patient had previously received 4 cycles of chemotherapy
with bleomycin and cisplatin; his preoperative physical exam and laboratory evaluation including pulmonary function
tests were unremarkable. His intraoperative anesthetic course was uneventful. The blood loss during surgery was
approximately 5000 cc, and he received 12 units PRBC, 2 units FFP, 8 units Platelets, 10 L crystalloid and 500cc
albumin. Postoperatively the patient was admitted to the ICU and ventilated overnight. Eight to ten hours postoperatively,
the patient's blood pressure dropped to 80/60 - 90/70. He received multiple fluid boluses and was started on low
dose doparnine. His hematocrit was unchanged. His blood pressure remained in the 90?100 range systolic with a heart
rate of 110-120 overnight and he was extubated the following morning. On the second postoperative day, the dopamine
dose was increased to 5-7mcg/kg/min and multiple fluid boluses were again given to maintain the mean blood pressure
at 80mmHg. On the third postoperative day the patient again became hemodynamically unstable with systolic blood
pressure 70-90mmHg. The patient's hematocrit remained stable and he received additional fluid boluses. Despite
aggressive hydration, the blood pressure dropped to 60mmHg systolic. Urine output varied from 20-30 cc/hr despite
addition of diuretics. His heart rate rose to 140 and the dopamine was increased to 10 mcg/kg/min. At this point
the patient was 6 liters positive in the postop period and appeared very edematous. On the evening of the third
postop day blood pressures fell to 50mmHg systolic and the patient became anuric. The dopamine infusion was increased
to 15 mcg/kg/min. The patient's saturation decreased to the mid 80's and he was given epinephrine boluses and intubated.
He remained hypotensive on epinephrine and dopamine infusions. Adrenal insufficiency was suspected and the patient
received hydrocortisone 100mg bolus and then 100mg q8h. The patient's hemodynamics dramatically improved after
hydrocortisone replacement and the dopamine was discontinued. The patient received hemodialysis for three days.
He was extubated on postoperative day 6. Renal function improved. The postoperative pathology report indicated
that the left adrenal gland was incidentally removed during the surgery. A cosyntropin (synthetic ACTH) stimulation
test was performed to assess adrenal function and was consistent with adrenal insufficiency. The patient was discharged
on hydrocortisone on postoperative day 14.
Discussion:
Adrenal insufficiency is a rare complication in patients undergoing RPLND. Here we present a case of postoperative
acute adrenal insufficiency following RPLD, with incidental left adrenalectomy. Adrenal dysfunction may result
from contralateral adrenal gland injury secondary to intraoperative hemorrhage, infarction or ischemia. The diagnosis
requires a high index of suspicion, since the clinical signs and symptoms are nonspecific. Hemodynamic instability
in young patients with poor response to fluid resuscitation in the absence of cardiac causes must alert the physician
to possible adrenal insufficiency that must be treated with intravenous corticosteroid preparation. In this patient,
hemodynamic instability during postoperative period was the only apparent sign of adrenal insufficiency.