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S Tisherman

Publications and source records attributed to S Tisherman.

13 recordsLinked to original sources
PubMed2000

Critical care medicine education of surgeons: recommendations from the Surgical Section of the Society of Critical Care Medicine.

PERSPECTIVE: The role of surgeons in critical care medicine has a long and esteemed past. The presence of surgeons in intensive care units provides specific insights and perspectives to the care of surgical patients sometimes not fully appreciated by the non-surgical practitioners caring for the same patients. The training and education of surgeons is becoming more complex, fragmented, and lengthy. The knowledge base and skill set required to manage critically ill or injured surgical patients is also becoming more extensive but has the potential of becoming lost in the process of providing the overall educational program for surgical trainees. Simultaneously, nonsurgical specialties are continuing to train individuals with special skills in critical care medicine and the concept of "hospitalists" is becoming more accepted by institutions across the United States. The certification exams in critical care medicine remain under the aegis of the individual medical specialty boards, and there is still not a unified examination process in critical care. Surgeons, in particular, have tremendous pressures these days to spend more clinical time in the operating room, and the task of consistently conducting high quality research is also becoming arduous. This list of reasons could continue but are simply examples for why surgeons need to spend focused attention on how best to train and educate upcoming surgical trainees in regards to the principles of critical care medicine. The critically ill or injured patients need this focused attention and the specialty of surgical critical care medicine needs this attention. The Surgical Section of the Society of Critical Care Medicine has developed this position statement in the hopes that ongoing discussion and refinement of this particular aspect of surgery will continue on several levels.

Critical Care↗
PubMed1998

Prolonged severe hemorrhagic shock and resuscitation in rats does not cause subtle brain damage.

OBJECTIVE: Some patients who survived severe hemorrhagic shock (HS) seem to exhibit persistent subtle neurobehavioral deficits. This finding is of concern if limited hypotensive fluid resuscitation is applied in hypotensive victims with penetrating trauma. This study was designed to determine whether subtle brain damage would occur in rats after severe prolonged HS. We hypothesized that rats surviving HS with mean arterial pressure (MAP) controlled at 40 mm Hg for 60 minutes would recover with slight permanent brain damage in terms of cognitive function without morphologic loss of neurons and that rats surviving HS with MAP at 30 mm Hg for 45 minutes (60 minutes were not tolerated) would have grossly abnormal brain function and loss of neurons. METHODS: Under light nitrous oxide-halothane anesthesia, spontaneously breathing rats underwent MAP-controlled HS (HS phase I), volume resuscitation to normotension and invasive monitoring to 60 minutes (resuscitation phase II), and observation to 10 days with detailed assessment of cognitive function (observation phase III). Five conscious rats served as normal controls. Three treatment groups were compared: group 1, shams (11 of 12 rats survived to 10 days); group 2, HS at MAP 40 mm Hg for 60 minutes (10 of 17 rats survived); group 3, HS at 30 mm Hg for 45 minutes (10 of 14 rats survived). RESULTS: On post-HS day 10, all normal controls and all survivors of all three groups were functionally normal with overall performance category = 1 (normal) (overall performance category 1 = normal, 5 = death) and neurologic deficit scores < or = 7% (neurologic deficit scores 0-10% = normal, 100% = brain death). Post-HS beam balance, beam walking, and Morris water maze test results in HS groups 2 and 3 showed latencies not significantly different from those in shams and normal controls. Light microscopic scoring of five selectively vulnerable brain regions and other regions in five coronal sections revealed no ischemic (pyknotic, shrunken, eosinophilic) neurons in any of the survivors to 10 days. There was no statistical difference between normal controls, sham animals, and both HS groups in the number of normal neurons counted in the hippocampal CA-1 region in the 10-day survivors. All nonsurvivors died with intestinal necrosis. CONCLUSION: HS at MAP 40 mm Hg for 60 minutes or MAP 30 mm Hg for 45 minutes does not cause subtle functional or histologic brain damage in surviving rats. Controlling MAP at 30 mm Hg carries a risk of sudden cardiac arrest. These data suggest that limited fluid resuscitation, to maintain MAP at about 40 mm Hg, as recommended for victims of penetrating trauma with uncontrolled HS, is safe for the brain.

Animals↗
PubMed1997

Hypothermia and minimal fluid resuscitation increase survival after uncontrolled hemorrhagic shock in rats.

OBJECTIVE: To test the hypothesis that protective-preservative moderate hypothermia during uncontrolled hemorrhagic shock (UHS) in rats increases survival. DESIGN: Randomized outcome study in rats. MATERIALS AND METHODS: UHS phase I of 90 minutes, with initial withdrawal of 3 mL/100 g of blood plus tail amputation, was followed by hemostasis and all-out resuscitation phase II from 90 to 150 minutes, and observation phase III to 72 hours. Forty male rats under light anesthesia and spontaneous breathing were randomized into four groups: Group 1 received no fluid resuscitation during UHS and normothermia (37.5 degrees C) throughout. Group 2 received no fluid resuscitation and hypothermia (30 degrees C) from 15 to 120 minutes. Group 3 received lactated Ringer's solution to maintain mean arterial pressure at 40 mm Hg during UHS and normothermia. Group 4 received lactated Ringer's solution to a mean arterial pressure of 40 mm Hg during UHS and hypothermia from 15 to 120 minutes. RESULTS: UHS phase I was survived by 0 of 10 rats in group 1, 7 of 10 in group 2, 5 of 10 in group 3, and 10 of 10 in group 4 (p < 0.01 for group 1 vs. 2, 3, or 4; p < 0.05 for group 4 vs. 3). Survival to 72 hours was achieved by 0 of 10 rats in group 1, 3 of 10 in group 2 (p < 0.001 vs. group 1), 1 of 10 in group 3, and 7 of 10 in group 4 (p < 0.001 vs. group 1, and p < 0.01 vs. group 3). All 72-hour survivors were neurologically normal. Necropsies in rats that died early during phase III showed edema and gastrointestinal hemorrhages. CONCLUSIONS: Moderate hypothermia or limited (hypotensive) fluid resuscitation --best both combined--increases survival during and after UHS in rats.

Animals↗
PubMed1996

Germline mutations in the Von Hippel-Lindau disease (VHL) gene in families from North America, Europe, and Japan.

Germline mutation analysis was performed in 469 VHL families from North America, Europe, and Japan. Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected. Most of the germline VHL mutations (124/137) occurred in 1-2 families; a few occured in four or more families. The common germline VHL mutations were: delPhe76, Asn78Ser, Arg161Stop, Arg167Gln, Arg167Trp, and Leu178Pro. In this large series, it was possible to compare the effects of identical germline mutations in different populations. Germline VHL mutations produced similar cancer phenotypes in Caucasian and Japanese VHL families. Germline VHL mutations were identified that produced three distinct cancer phenotypes: (1) renal carcinoma without pheochromocytoma, (2) renal carcinoma with pheochromocytoma, and (3) pheochromocytoma alone. The catalog of VHL germline mutations with phenotype information should be useful for diagnostic and prognostic studies of VHL and for studies of genotype-phenotype correlations in VHL.

Adrenal Gland Neoplasms↗
PubMed1995

Uncontrolled hemorrhagic shock outcome model in rats.

During uncontrolled hemorrhagic shock (UHS) in acute animals models, attempts to achieve normotension with i.v. fluid resuscitation (FR) caused further bleeding and higher acute mortality. In the absence of a published clinically realistic long-term animal outcome study of UHS, we developed such a model in rats. In the preliminary study, phase I of the model involved 60 min of simulated 'pre-hospital' UHS by tail amputation and different FR regimens. Phase II involved 120 min of simulated 'hospital' treatment with hemostasis and all-out FR, including blood infusion. Phase III involved observing recovery and survival to 72 h (3 days). Rats were maintained under very light N2O-O2-halothane anesthesia and spontaneous breathing via mask during phases I and II and were awake during phase III. Tail amputation-induced UHS alone, studied in 4 groups of 10 rats each, resulted in unpredictable spontaneous hemostasis and great variability in shed blood volume, severity of shock, and mortality. The final model, which achieved consistent blood loss and outcome, included an initial volume-controlled hemorrhage of 3 ml/100 g over 15 min and untreated HS for another 15 min, followed by tail amputation for UHS over another 60 min. This phase I of 90 min was followed by phase II of 60 min. In group 1, without FR in phases I and II, all 10 rats died by 12 h. In group 2, without FR in phase I and hemostasis plus all-out FR with lactated Ringer's solution and blood to hematocrit (Hct) 30% in phase II, 5 of 10 rats died at the end of phase I and 9 of 10 died at the end of phase III. This final volume-initiated UHS model may be suitable for comparing different pre-hospital treatment modalities in terms of outcome.

Animals↗
PubMed1995

Improved outcome with fluid restriction in treatment of uncontrolled hemorrhagic shock.

BACKGROUND: Recent studies have challenged current guidelines for prehospital fluid resuscitation. However, long-term studies evaluating the consequences of fluid restriction in uncontrolled hemorrhagic shock are lacking. This study was done to examine the long-term effects of deliberate hypotension in the treatment of uncontrolled hemorrhage. STUDY DESIGN: Uncontrolled hemorrhagic shock was produced in 40 rats by a preliminary bleed (3 mL per 100 g) followed by 75 percent tail amputation. Experimental design consisted of three phases: a "prehospital phase" (90 minutes of uncontrolled bleeding with or without treatment with lactated Ringer's [LR] solution), followed by a "hospital phase" (60 minutes, including control of hemorrhage and fluid resuscitation including blood), and a three day observation phase. Forty rats were studied in four treatment groups (ten rats per group). Group 1 consisted of untreated controls (no resuscitation). Group 2 had no fluid during the prehospital phase. Group 3 had prehospital resuscitation to a mean arterial pressure (MAP) of 40 mm Hg with LR, and group 4 had prehospital resuscitation to MAP of 80 mm Hg with LR. Groups 2, 3, and 4 received fluid and blood to MAP of 80 mm Hg and hematocrit of 30 percent in the hospital phase. RESULTS: All rats in group 1 (untreated) died within 2.5 hours. Five rats in group 2 (no prehospital FR) survived 90 minutes; however, only one survived three days. In group 3, all ten rats survived 2.5 hours and six survived three days. In group 4, eight rats died within 90 minutes, but none survived long-term. Blood loss (mL per 100 g) for each group was 3.75 0.6 for group 1, 3.35 0.1 for group 2, 4.15 0.8 for group 3, and 8.45 0.6 for group 4, (p < 0.05, group 4 compared with groups 1, 2, and 3). CONCLUSIONS: Attempts to achieve normal MAP during uncontrolled bleeding increased blood loss, hemodilution and mortality. Hypotensive resuscitation resulted in less acidemia and improved long-term survival.

Animals↗
PubMed1993

Systematic development of cerebral resuscitation after cardiac arrest. Three promising treatments: cardiopulmonary bypass, hypertensive hemodilution, and mild hypothermia.

Since 1970 we have investigated postischemic anoxic encephalopathy and potential treatments for cerebral resuscitation after cardiac arrest by cardiopulmonary-cerebral resuscitation (CPCR). The post-resuscitation syndrome has been studied at the levels of cell, organ, organism and community. Short-term and long-term models in rats, dogs, and monkeys have been developed, and an international multicenter randomized clinical trial mechanism was established. Clinical studies disproved the 5-min limit of reversible cardiac arrest and yielded other valuable data on treatments and prognostication. Thiopental loading or calcium entry blocker therapy (lidoflazine) gave no significant improvement in patients. Free radical scavengers are under investigation in the laboratory. We hypothesize that post-arrest perfusion failure and necrotizing cascades require etiology-specific combination treatments. Standard (control) therapy in a current dog model of cardiac arrest (no flow) of 12.5-20 min, reperfusion with cardiopulmonary bypass, and intensive care for 72-96 h has consistently resulted in survival with brain damage. After ventricular-fibrillation (VF) arrest of 17 min, moderate hypothermia (28-32 degrees C) inconsistently improved cerebral outcome. After VF arrest of 12.5 min, hypertension plus hemodilution normalized the local (multifocal) cerebral hypoperfusion post-arrest and, again, inconsistently improved cerebral outcome. Additional mild hypothermia (34-36 degrees C), however, consistently improved cerebral outcome, whether induced before or during and after arrest.

Animals↗
PubMed1992

Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.

BACKGROUND AND PURPOSE: Mild cerebral hypothermia (34 degrees C) induced immediately after cardiac arrest improves outcome. Deep postarrest hypothermia (15 degrees C) has not been studied. METHODS: We used our dog model of normothermic ventricular fibrillation (no blood flow) of 12.5 minutes, reperfusion by brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 72 hours. Head surface cooling and bypass cooling were performed from start of reperfusion to 1 hour. Five groups of six dogs each were compared: group I, normothermic controls; group II, deep hypothermia (15 degrees C); group III, moderate hypothermia (30 degrees C); group IV, mild hypothermia (34 degrees C); and group V, mild hypothermia with head surface cooling begun during no flow. RESULTS: In control group I, five dogs remained comatose (overall performance category [OPC] 4) and one severely disabled (OPC 3). In group II, four dogs achieved OPC 4 and two dogs OPC 3 (NS versus group I). Compared with group I, OPCs were better in group III (p less than 0.05), group IV (p less than 0.05), and group V (p less than 0.05). Neurological deficit scores were also better in groups III, IV, and V than in groups I or II (p less than 0.05). Total brain histological damage scores were better in group III (p = 0.02), group IV (p = 0.06), and group V (p less than 0.05) than in group I. In group II, OPC and neurological deficit scores were the same and histological damage scores numerically worse than in group I and all were worse than in groups III, IV, and V (p less than 0.05). Cardiovascular complications and myocardial morphological damage in groups II and III were worse than in groups I, IV, and V (p less than 0.05). CONCLUSIONS: Mild or moderate cerebral hypothermia induced immediately after cardiac arrest improves cerebral outcome, more likely when initiated during arrest, whereas deep postarrest hypothermia can worsen cerebral and cardiac outcome.

Animals↗
PubMed1991

Mild hypothermic cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs.

BACKGROUND AND METHODS: This study was designed to explore the effect of mild cerebral and systemic hypothermia (34 degrees C) on outcome after prolonged cardiac arrest in dogs. After ventricular fibrillation with no flow of 10 min, and standard external CPR with epinephrine (low flow) from ventricular fibrillation time of 10 to 15 min, defibrillation and restoration of spontaneous normotension were between ventricular fibrillation time of 16 and 20 min. This procedure was followed by controlled ventilation to 20 hr postarrest and intensive care to 72 hr postarrest. In control group 1 (n = 10), core temperature was 37.5 degrees C; in control group 2 (n = 10), cooling was started immediately after restoration of spontaneous normotension; and in group 3 (n = 10), cooling was initiated with start of CPR. Cooling was by clinically feasible methods. RESULTS: Best overall performance categories achieved (1 = normal; 5 = brain death) were better in group 2 (p = .012) and group 3 (p = .005) than in group 1. Best neurologic deficit scores were 36 +/- 14% in group 1, 22 +/- 15% in group 2 (p = .02), and 19 +/- 18% in group 3 (p = .01). Brain histopathologic damage scores were also lower (better) in groups 2 (p = .05) and 3 (p = .03). Myocardial damage was the same in all three groups. CONCLUSION: Mild cerebral hypothermia started during or immediately after external CPR improves neurologic recovery.

Animals↗
PubMed1990

Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs.

We previously found mild hypothermia (34-36 degrees C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34 degrees C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5 degrees C was reversed with cardiopulmonary bypass and defibrillation in less than or equal to 5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.

Animals↗
PubMed1985

Resuscitation of dogs from cold-water submersion using cardiopulmonary bypass.

In cold-water drowning, attempts at restoration of spontaneous circulation (ROSC) by external cardiopulmonary resuscitation (CPR) often fail. We explored the longest period of asphyxial cardiac arrest from cold-water submersion (without inhalation of water) from which ROSC is possible using cardiopulmonary bypass (CPB). In 19 lightly anesthetized dogs the tracheal tube was clamped (simulating laryngospasm) and the dogs were immersed in ice water from 20, 40, 60, 90, or 120 minutes. Cardiac arrest occurred after six to 11 minutes of submersion. At start of resuscitation, rectal temperature ranged from 21 C (after 60 minutes) to 34 C (after 20 minutes of submersion), and cerebral temperature was between 7 C (after 120 minutes) and 27 C (after 20 minutes submersion). Resuscitation attempts were performed according to protocol in 16 dogs, using only CPB by venoarterial pumping with an oxygenator and a heat exchanger. Priming was with 400 to 800 mL Dextran 40 and Ringer's solution 1:1 plus heparin. CPB flows were 10 mL/kg/min, and they increased to achieve normotension and return of rectal temperature to 32 C. After one-half to three hours, of CPB, ROSC was successful in 75%. This percentage included one of three dogs after 90 minutes submersion, but not in the one dog after 120 minutes submersion. Spontaneous breathing and EEG activity returned in 56% at two to 24 hours, after 20 to 90 minutes of submersion. Failure of ROSC attempts apparently were due to clotting in large vessels during arrest and capillary leakage during reperfusion. CPB is effective for ROSC after prolonged hypothermic cardiac arrest, and it should be evaluated in animal outcome studies.

Animals↗