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Biomedical subjects

P K Schoenwald

Publications and source records attributed to P K Schoenwald.

18 recordsLinked to original sources
PubMed2000

Intraoperative management of renal function in the surgical patient at risk. Focus on aortic surgery.

Although the search for effective methods of renal prophylaxis during aortic surgery spans many decades, definitive answers are scarce. The literature is voluminous, yet the amount of work clearly relevant to the specific clinical situation of perioperative prophylaxis is small. Given the significant morbidity and subsequent mortality involved with perioperative ARF, it is difficult to sit back and do nothing when pharmacologic agents empirically are believed to possibly benefit the patient. Care must be taken to apply data from different clinical scenarios in the literature to the situation at hand. Drugs felt to be innocuous, even in low doses, may be insidiously counterproductive or damaging if they are not managed properly. Maintaining an adequate preload and stable hemodynamics seems to be the most logical universal approach at this time. Furosemide treatment without maintaining an adequate volume status once diuresis commences may be detrimental, which is true with the diuretic effects induced by mannitol or dopamine. The tachycardia resulting from a relative hypovolemia and from the beta effects of dopamine can cause myocardial ischemia from increased oxygen demand. Low urine output does not portend a negative outcome in the face of an adequate intravascular volume any more than an induced diuresis prevents renal injury. Currently, minimization of renal ischemia and maintenance of an adequate intravascular volume and renal hemodynamics are the keys to optimizing renal outcome during aortic surgery. Other maneuvers are not definitive and should be cautiously undertaken.

Acute Kidney Injury↗
PubMed2000

Small-dose dopamine increases epidural lidocaine requirements during peripheral vascular surgery in elderly patients.

UNLABELLED: We studied 20 patients over the age of 65 yr undergoing prolonged peripheral vascular surgery under continuous lidocaine epidural anesthesia, anticipating that the increased hepatic metabolism caused by small-dose IV dopamine would lower plasma lidocaine concentrations. Subjects were assigned (random, double-blinded) to receive either a placebo IV infusion or dopamine, 2 microg. kg(-1). min(-1) during and for 5 h after surgery. Five minutes after the IV infusion was started, 20 mL of 2% lidocaine was injected through the epidural catheter. One-half hour later, a continuous epidural infusion of 2% lidocaine at 10 mL/h was begun. The epidural infusion was temporarily decreased to 5 mL/h or 5 mL boluses were added to maintain a T8 analgesic level. Arterial blood samples were analyzed for plasma lidocaine concentrations regularly during and for 5 h after surgery. Plasma lidocaine concentrations increased continuously during the epidural infusion and, despite wide individual variation, were similar for the two groups throughout the observation period. During the observation period, the mean maximal plasma lidocaine concentration was 5.8 +/- 2.3 microg/mL in the control group and 5.7 +/- 1.2 microg/mL in the dopamine group. However, the mean hourly lidocaine requirement during surgery was significantly different, 242 +/- 72 mg/h for control and 312 +/- 60 mg/h for dopamine patients (P < 0.03). At the end of Hour 4, the last period when all 20 patients were still receiving the epidural lidocaine infusion, the total lidocaine requirement was significantly different, 1088 +/- 191 mg for the control group and 1228 +/- 168 mg for the dopamine group (P < 0.05). Despite very large total doses of epidural lidocaine (1650 +/- 740 mg, control patients, and 1940 +/- 400, dopamine patients) mean maximal plasma concentrations remained below 6 microg/mL, and no patient exhibited signs or symptoms of toxicity. We conclude that small-dose IV dopamine increased epidural lidocaine requirements, presumably as a consequence of increased metabolism. IMPLICATIONS: We tested dopamine, a drug that increases liver metabolism of the local anesthetic lidocaine to determine if it would prevent excessively large amounts of lidocaine in the blood during prolonged epidural anesthesia in elderly patients. Dopamine did not alter the blood levels of lidocaine, but it did increase the lidocaine dose requirement to maintain adequate epidural anesthesia.

Adjuvants, Anesthesia↗
PubMed1998

Cauda equina syndrome after spinal anaesthesia in a patient with severe vascular disease.

PURPOSE: Spinal anaesthesia is selected for many lower extremity surgical procedures each year in the United States with a high degree of safety and efficacy. Even when adverse neurological outcomes have occurred, anatomical abnormality or coagulopathy have been implicated in the majority of cases. Epinephrine is used in high concentrations in many of these anaesthetics to increase the duration and intensity of the block. Although epinephrine is known to decrease spinal cord blood flow, its use in normal patients has not caused complications. We report a case where spinal anaesthesia with bupivacaine and epinephrine resulted in anterior spinal artery compromise and the development of a cauda equina syndrome postoperatively. CLINICAL FEATURES: A 57-yr-old man with severe coronary artery and peripheral vascular disease was scheduled for incision and drain of an abscess of the left thigh. He received an atraumatic dural puncture and injection of 12.5 mg bupivacaine with 0.2 ml 1:1000 epinephrine. During onset, he experienced a severe, painful sensation of the thighs which resolved with development of the block. Postoperatively, he was noted to have exacerbation of proximal muscle weakness and decreased perineal sensation and rectal tone. Subsequent EMG studies demonstrated proximal neuron loss consistent with cauda equina syndrome, presumed to be related to insufficiency of the anterior spinal artery. CONCLUSION: Routine use of epinephrine in spinal anaesthesia for patients with multi-organ vascular disease should be considered carefully because of the possibility of vascular insufficiency of the spinal cord which would be exaggerated by the vasoconstrictive effect of epinephrine.

Anesthesia, Spinal↗
PubMed1998

Ischemic liver dysfunction after elective repair of infrarenal aortic aneurysm: incidence and outcome.

OBJECTIVE: To assess the frequency of early postoperative liver dysfunction in patients undergoing elective infrarenal aortic aneurysm repair, their hospital course, and outcome. DESIGN: A retrospective case-control study. SETTING: A single tertiary referral center. PARTICIPANTS: A review of medical records of 942 consecutive asymptomatic patients with normal preoperative liver function test results who had elective infrarenal aortic aneurysm repair with infrarenal aortic cross-clamping. The authors selected all patients who had an acute increase in serum hepatic enzyme levels (minimum fivefold increase in aspartate aminotransferase [AST] and twofold increase in lactate dehydrogenase [LDH] levels) within the first 7 perioperative days (study patients). The control group consisted of 42 patients with normal postoperative liver function test results, matched by age, sex, and year of surgery to study patients. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Aortic cross-clamping times, lowest intraoperative blood pressure, duration of hypotension (systolic blood pressure < or = 95 mmHg), lowest intraoperative base deficit, and estimated blood loss were compared between control and study patients. The study also analyzed perioperative metabolic, hemostatic, hepatic, and renal function variables; the intraoperative course; postoperative complications; and inhospital outcome. Fourteen of 942 patients (1.5%) comprised a study group. In 11 patients (1.2%), AST and LDH levels moderately increased, and three patients (0.3%) developed changes consistent with a diagnosis of acute ischemic hepatitis (AIH). In all patients, the serum liver enzyme levels peaked between 24 and 72 postoperative hours. Three patients with AIH developed concomitant acute renal failure; one had associated disseminated intravascular coagulation (DIC) and died. Of 11 patients with moderate increases, one subsequently developed multisystem organ failure and died. The overall in-hospital mortality rate for patients with postoperative liver dysfunction was 14% (2/14) and for the control group it was 2.3% (1/42). The duration of hypotension and metabolic acidosis were more pronounced in patients who postoperatively developed liver dysfunction (both p < 0.001); however, study and control patients did not differ in the duration of aortic cross-clamping, lowest intraoperative blood pressure, or estimated blood loss. CONCLUSION: Liver enzyme levels acutely increased in 1.5% of patients after elective infrarenal aortic aneurysm repair with infrarenal cross-clamping. In patients with moderately elevated serum liver enzyme levels, postoperative recovery was relatively uncomplicated, whereas all three patients with AIH developed acute renal failure and had a more complicated postoperative course. Those with postoperative liver dysfunction had a longer duration of intraoperative hypotension and more pronounced metabolic acidosis.

Aged↗
PubMed1995

The hemodynamic responses to an intravenous test dose in vascular surgical patients.

The study was designed to investigate the hemodynamic responses to intravenous (IV) injections of various epidural test doses in vascular surgical patients to determine whether previously established criteria in healthier populations were valid in this inherently sicker population. A double-blind, prospective randomized study was performed on 50 patients, not receiving beta-adrenergic antagonists, presenting for vascular surgery and requiring an arterial line. Patients were randomly assigned to receive a 3-mL injection of one of five solutions, either saline (Group 1), lidocaine 45 mg (Group 2), lidocaine 45 mg and epinephrine 5 micrograms (Group 3), lidocaine 45 mg and epinephrine 10 micrograms (Group 4), or lidocaine 45 mg and epinephrine 15 micrograms (Group 5). After injection, a blinded observer recorded arterial blood pressure and heart rate (HR) every 15 s for 3 min. The changes in HR, systolic (SBP), mean (MBP), and diastolic (DBP) blood pressure as well as time to maximum change were analyzed both within and between groups. Only Group 5 had significant within-group changes for all hemodynamic variables measured. Only in the comparison between Groups 1 and 5 and between Groups 2 and 5 were there significant changes in both HR and SBP. The mean increase in HR and SBP within Group 5 was 17.0 +/- 5.9 bpm and 31.0 +/- 10.5 mm Hg, respectively. No differences were found between groups for time to maximum change for HR and SBP which for Group 5 were 64.5 +/- 37.4 s and 90.0 +/- 56.7 s, respectively. To achieve 100% sensitivity and specificity for HR increase, the criterion established was > or = 9 bpm.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

The effect of posture on the induction of epidural anesthesia for peripheral vascular surgery.

BACKGROUND AND OBJECTIVES: A study was done to determine whether a difference existed in the quality and time to maximum anesthesia between the induction of lumbar epidural anesthesia in the sitting and supine position in patients undergoing infrainguinal arterial reconstruction. METHODS: An epidural catheter was inserted at L3-L4 in 40 patients who were randomly assigned to two groups. In group 1, with the patient sitting, 3 mL lidocaine 1.5% with 5 micrograms/mL epinephrine was given as a test dose, followed 3 minutes later by 12 mL bupivacaine 0.75% injected over 2 minutes through the catheter. After remaining in the sitting position for 5 minutes, the patient was placed supine and the quality of anesthesia assessed at 3-minute intervals for 30 minutes. Anesthesia was assessed by loss of sensation to pinprick and the Bromage scale for loss of motor function. In group 2, after placement of the catheter, the patient was immediately placed supine, the same doses of local anesthesia were given at the same time intervals as in group 1, and the onset of anesthesia was similarly assessed. In addition to a comparison between groups in the quality and time to maximum anesthesia, a correlation was sought between these variables and the age, weight, height, and body surface area (BSA) of the patients in each group. RESULTS: The demographically similar groups showed no difference in maximum cephalad spread of anesthesia (median, interquartile range; group 1: T4, T2.5-T6; group 2: T4, T2.5-T7), motor block (group 1: 3, 2-4; group 2: 4, 4-6), or time to maximum motor block (mean +/- SD; group 1, 17.4 +/- 8.7 minutes; group 2, 17.9 +/- 6.8 minutes). The time to maximum cephalad spread of anesthesia was shorter in group 1 (13.8 +/- 6.9 minutes; group 2, 18.6 +/- 6.6 minutes; P = .03). Neither the age nor weight of the patients in either group had any influence on the quality and time to maximum anesthesia. There was, however, a significant correlation between the height (r = 0.48, P = .0303) and BSA (r = 0.48, P = .0318) of the patients in group 1 and the time to maximum cephalad spread of anesthesia. CONCLUSIONS: When lumbar epidural anesthesia was induced in the sitting rather than supine position, the time to maximum cephalad spread was shorter and correlated directly with the height and BSA of the patient. The position of the patient during induction had no effect on the final level of cephalad spread and degree of motor block.

Age Factors↗