Hamdy Awad

Anesthetic considerations for robotic prostatectomy: a review of the literature.

Since the first robotic prostatectomy in 2000, the number of prostatectomies performed using robot-assisted laparoscopy has been increasing. As of 2009, 90,000 robotic radical prostatectomies were performed worldwide, and 80% of all radical prostatectomies performed in the United States were performed robotically. Robotic prostatectomy is becoming more common globally because of the many advantages offered to patients, primarily due to the minimally invasive nature of the procedure. Several new perioperative concerns and challenges for anesthesiologists and are described.

The evolving management of acute right-sided heart failure in cardiac transplant recipients.

Avoidance of the clinical syndrome of acute right-sided heart failure after heart transplantation is, unfortunately, not possible. Clinical experience and the literature certainly suggest that a significant factor in the successful management of right ventricular (RV) failure is recipient selection. Moreover, threshold hemodynamic values beyond which RV failure is certain to occur and heart transplantation is contraindicated do not exist. Nor are there values below which RV failure is always avoidable. Acute RV failure will remain a difficult and ever-present clinical syndrome in the transplant recipient. Goals in the treatment of this clinical problem include: 1. Preserving coronary perfusion through maintenance of systemic blood pressure. 2. Optimizing RV preload. 3. Reducing RV afterload by decreasing pulmonary vascular resistance (PVR). 4. Limiting pulmonary vasoconstriction through ventilation with high inspired oxygen concentrations (100% FiO(2)), increased tidal volume and optimal positive end expiratory pressure ventilation. Inhaled nitric oxide is recommended before leaving the operating room in cases where the initial therapies have had little impact. Intra-aortic balloon counterpulsation is employed in patients with impaired left ventricular (LV) function and may be of benefit in patients with RV dysfunction resulting from ischemia, preservation injury or reperfusion injury. Optimal LV function reduces RV afterload and PVR. A proactive decision regarding RV assist device implantation is made before leaving the operating room and is highly dependent upon overall hemodynamics, size and function of the ventricles as seen on transesophageal echocardiography, renal function and surgical bleeding. Only through careful preoperative planning can this life-threatening condition be managed in the postoperative period.

Peripheral and spinal actions of opioids in the blockade of the autonomic response evoked by compression of the inflamed knee joint

Background Three types of opioid receptors, micro, delta, and kappa, are present in the periphery and in the central nervous system. In contrast to the effects in the central nervous system, the antinociceptive action of opioids in the periphery is not as well characterized. The effects of intraarticular, spinal, and intramuscular injections of micro, delta, and kappa opioid agonists on the autonomic response evoked by compression of an inflamed knee joint were evaluated. Methods In halothane‐anesthetized rats, arthritis was induced by injecting kaolin and carrageenan into the right knee joint. Standardized compression of the knee joint by inflation of a pediatric blood pressure cuff to 200 mmHg for 2 min produced a reliable stimulus‐dependent hypertension (Delta = 13 mmHg). Drugs were delivered intramuscularly, intrathecally through a chronic catheter, or intraarticularly into the right knee joint. The drug injection was performed 4 hr after induction of the inflammation. Results The intrathecal administration of micro, delta, and kappa agonists resulted in a dose‐dependent blockade of the cuff‐evoked increase in blood pressure. The order of intrathecal drug activity on the compression‐evoked blood pressure responses with median effective dose (ED50) was sufentanil (0.02 nmol; micro) > PD117302 (0.5 nmol; kappa); spiradoline (1.5 nmol; kappa) morphine (2.4 nmol; micro) > DADL (15 nmol; delta); DPDPE (18 nmol; delta) > U‐50,488H (620 nmol; kappa) > naloxone = 0. The intraarticular administration of micro and kappa, but not delta agonists, produced a dose‐dependent blockade of a compression‐evoked increase in blood pressure, with the order of drug activity (ED50) as follows: sufentanil (0.04 micro mol) > PD117302 (0.3 micro mol); spiradoline (0.8 micro mol), morphine (0.9 micro mol) > U‐50,488H (0.9 micro mol) > DPDPE (> 5 micro mol); DADL (> 18 micro mol) > naloxone = 0. Intramuscular injection of these agonists caused suppression, with the order of drug activity (ED50) as follows: sufentanil (0.2 micro mol) > PD117302 (2 micro mol); spiradoline (11 micro mol) morphine (9 micro mol) > DPDPE (> 5 micro mol); DADL (18 micro mol) > U‐50,488H (22 micro mol) > naloxone = 0. All intraarticular effects were reversible by injecting naloxone intramuscularly, with the ordering of naloxone potency against equiactive doses of morphine > U50,488H. Conclusions The activity of the respective agonists and the intraarticular > intramuscular ordering of systemic potency in this model indicate that opioids, by an action at micro and kappa, can exert a direct antihyperalgesic action at the terminals of primary afferents projecting to a region of inflammation. These observations offer strong support for a peripheral action of opioids in certain states in inflammation‐induced hyperalgesia.

A Mouse Model of Ischemic Spinal Cord Injury with Delayed Paralysis Caused by Aortic Cross-clamping

Background:Spinal cord ischemia and paralysis are devastating perioperative complications that can accompany open or endovascular repair surgery for aortic aneurysms. Here, we report on the development of a new mouse model of spinal cord ischemia with delayed paralysis induced by cross-clamping the descending aorta. Methods:Transient aortic occlusion was produced in mice by cross-clamping the descending aorta through a lateral thoracotomy. To establish an optimal surgical procedure with limited mortality, variable cross-clamp times and core temperatures were tested between experiments. Results:The onset of paresis or paralysis and postsurgical mortality varied as a function of cross-clamp time and core temperature that was maintained during the period of cross-clamp. Using optimal surgical parameters (7.5-min cross-clamp duration at 33°C core temperature), the onset of paralysis is delayed 24–36 h after reperfusion, and more than 95% of mice survive through 9 weeks after surgery. These mice are further stratified into two groups, 70% (n = 19/27) of mice developing severe hind limb paralysis and the remaining mice showing mild, though still permanent, behavioral deficits. Conclusion:This new model should prove useful as a preclinical tool for screening neuroprotective therapeutics and for defining the basic biologic mechanisms that cause delayed paralysis and neurodegeneration after transient spinal cord ischemia.

Intracellular and extracellular expression of the major inducible 70kDa heat shock protein in experimental ischemia-reperfusion injury of the spinal cord

Inflammatory responses exacerbate ischemia-reperfusion (IR) injury of spinal cord, although understanding of mediators is incomplete. The major inducible 70kDa heat shock protein (hsp70) is induced by ischemia and extracellular hsp70 (e-hsp70) can modulate inflammatory responses, but there is no published information regarding e-hsp70 levels in the cerebrospinal fluid (CSF) or serum as part of any neurological disease state save trauma. The present work addresses this deficiency by examining e-hsp70 in serum and CSF of dogs in an experimental model of spinal cord IR injury. IR injury of spinal cord caused hind limb paraplegia within 2-3 h that was correlated to lumbosacral poliomalacia with T cell infiltrates at 3 d post-ischemia. In this context, we showed a 5.2-fold elevation of e-hsp70 in CSF that was induced by ischemia and was sustained for the following 3 d observation interval. Plasma e-hsp70 levels were unaffected by IR injury, indicating e-hsp70 release from within the central nervous system. A putative source of this e-hsp70 was ependymal cells in the ischemic penumbra, based upon elevated i-hsp70 levels detected within these cells. Results warrant further investigation of e-hsp70s potential to modulate spinal cord IR injury.

First evidence of sternal wound biofilm following cardiac surgery.

Management of deep sternal wound infection (SWI), a serious complication after cardiac surgery with high morbidity and mortality incidence, requires invasive procedures such as, debridement with primary closure or myocutaneous flap reconstruction along with use of broad spectrum antibiotics. The purpose of this clinical series is to investigate the presence of biofilm in patients with deep SWI. A biofilm is a complex microbial community in which bacteria attach to a biological or non-biological surface and are embedded in a self-produced extracellular polymeric substance. Biofilm related infections represent a major clinical challenge due to their resistance to both host immune defenses and standard antimicrobial therapies. Candidates for this clinical series were patients scheduled for a debridement procedure of an infected sternal wound after a cardiac surgery. Six patients with SWI were recruited in the study. All cases had marked dehiscence of all layers of the wound down to the sternum with no signs of healing after receiving broad spectrum antibiotics post-surgery. After consenting patients, tissue and/or extracted stainless steel wires were collected during the debridement procedure. Debrided tissues examined by Gram stain showed large aggregations of Gram positive cocci. Immuno-fluorescent staining of the debrided tissues using a specific antibody against staphylococci demonstrated the presence of thick clumps of staphylococci colonizing the wound bed. Evaluation of tissue samples with scanning electron microscope (SEM) imaging showed three-dimensional aggregates of these cocci attached to the wound surface. More interestingly, SEM imaging of the extracted wires showed attachment of cocci aggregations to the wire metal surface. These observations along with the clinical presentation of the patients provide the first evidence that supports the presence of biofilm in such cases. Clinical introduction of the biofilm infection concept in deep SWI may advance the current management strategies from standard antimicrobial therapy to anti-biofilm strategy.

Abdominal only CPR during cardiac arrest for a patient with an LVAD during resternotomy: A case report

We present a case in which a patient with a previous sternotomy and left ventricular assist device (LVAD) implantation developed cardiac arrest during resternotomy for LVAD exchange. The surgeon refused chest compressions for fear of potential damage to the inflow cannula directly beneath the sternum. The perioperative team had no alternatives to external cardiac massage other than rapid deployment of extra-corporeal membrane oxygenation for mechanical support, so the anesthesiologist advised the nursing personnel to perform abdominal only cardiopulmonary resuscitation while the surgeon performed a femoral bypass to cannulate the groin for extra-corporeal membrane oxygenation support.

Quaking and miR-155 interactions in inflammation and leukemogenesis

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas expression and the rate of Caspase3/7 activity, while increasing the levels of IL-1α, IL-1β and IL-6, and p38 phosphorylation. Similarly, the p38 pathway is also a target of QKI activity in chronic lymphocytic leukemia (CLL)-derived MEC2 cells. Finally, B-CLL patients show lower levels of QKI expression compared with B cells from healthy donor, and Qki is similarily downregulated with the progression of leukemia in Eμ-miR-155 transgenic mice. Altogether, these data implicate QKI in the pathophysiology of inflammation and oncogenesis where miR-155 is involved.

Endogenous Opioids in Wound-Site Neutrophils of Sternotomy Patients

Background Postoperative pain management is a critical aspect of patient care. The inflammatory state of the post-sternotomy surgical wound sensitizes nerve endings, causing pain. Unrelieved or improperly managed pain compromises wound healing. Peripheral opioid receptors play a major role in analgesia, particularly under inflammatory conditions where both opioid receptor expression and efficacy are increased. Leukocytic opioid peptides include β-endorphin (END), met-enkephalin (ENK), and dynorphin-A (DYN), with END and ENK being predominant. Methodology/Principal Findings This work represents the first study of inflammatory cells collected from post-sternotomy wounds of patients undergoing cardiac surgery including coronary artery bypass grafting (CABG). Wound fluid (WF) and cells were collected from sternal wounds using a JP Blake drain at 24, 48, and 72 hours post sternum closure. Anti-CD15 staining and flow cytometry revealed that polymorphonuclear neutrophils (PMN) are the predominant cells present in wound fluid collected post-surgery. Compared to peripheral blood (PB) derived PMN, significant increases in CD177+/CD66b+ PMN were observed suggesting activation of wound-site PMN. Such activation was associated with higher levels of opioid peptide expression in PMN derived from WF. Indeed, increased level of opioid peptides in sternal wound environment was noted 72 h post-surgery. We demonstrate that WF contains factors that can significantly induce POMC transcription in human PMNs. IL-10 and IL-4 were abundant in WF and both cytokines significantly induced POMC gene expression suggesting that WF factors such as IL-10 and IL-4 contribute towards increased opioid peptide expression in wound-site PMN. Conclusions/Significance This approach provided a unique opportunity to study the cross-talk between inflammation and opioid peptides in PMN at a sternotomy wound-site. Wound-site PMN exhibited induction of END and ENK. In addition, sternal wound fluid significantly induced END expression in PMN. Taken together, these data constitute first clinical evidence that human wound-site PMNs are direct contributors of opioids at the sternal wound-site.

Initial experience with off-pump left ventricular assist device implantation in single center: retrospective analysis

BackgroundWe hypothesize that implantation of left ventricular assist device through off-pump technique is feasible and has a comparable result to implantation on cardiopulmonary bypass and could improve one-year survival.MethodsThis retrospective, observational, single-center study was conducted on 29 consecutive patients at our institution who underwent off-pump left ventricular assist device implantation by a single surgeon.ResultsTwenty-seven procedures were performed successfully using the off-pump technique. The survival rate was 92% at 30 days, 76% at 90 days, and 67% at one year. We compared the one-year survival of different implantation periods, and divided our study into three time intervals (2004-2005, 2006, and 2007). There was a trend in reduction in number of deaths over one year that demonstrated a decrease in death rate from 50% to 17%, as well as improvement in our experience over time. However, this trend is not statistically significant (p = 0.08) due to limited sample size.ConclusionsBased upon our findings, off-pump left ventricular assist device implantation is a feasible surgical technique, and combining this technique with improved device technology in the future may provide even greater improvement in patient outcomes.