Intravenous Administration Of Mannitol Research Articles

Preoperative intravenous mannitol administration and its rationale before cataract surgery.

The purpose of this study is to assess the variations in anterior chamber depth (ACD), axial length (AXL), and intraocular pressure (IOP) in both phakic and pseudophakic eyes undergoing preoperative intravenous mannitol infusion. The study was conducted at the Ophthalmology Department of IRCSS Humanitas in Milan, Italy. This is a prospective and non-randomized study. 40 patients with phakic eyes and 40 patients with pseudophakic eyes scheduled for cataract surgery in their fellow eye were included. Prior to the surgery, comprehensive ophthalmic examinations were conducted, including IOP measurement, and bilateral biometry performed with Anterion® (Heidelberg Engineering GmbH, 69,115, Heidelberg, Germany). All patients received intravenous infusion of mannitol before the surgery. One hour after cataract extraction, the patients underwent the same set of examinations. We analyzed the changes AXL, ACD and IOP in the eye opposite to the one that underwent surgery. The comparison between preoperative and postoperative parameters showed no differences in AXL (p = 0.34 and p = 0.53) and in ACD (p = 0.38 and p = 0.31) in the phakic and in the pseudophakic group, respectively. Instead, a statistically significant difference was found between the mean preoperative and postoperative IOP (p = 0.02) for the phakic group and (p = 0.03) for the pseudophakic group. The administration of mannitol does not lead to any changes in the ACD and AXL, regardless of whether the eyes are phakic or pseudophakic. However, there is a statistically significant reduction in IOP. Nonetheless, it is important to consider the various side effects associated with mannitol infusion.

Intraoperative Intravenous Mannitol Administration Failed to Provide Added Value on Renal Functional Preservation After Partial Nephrectomy in Patients with Chronic Kidney Disease: A Matched Cohort Study.

Background: Previous randomized-controlled trials have demonstrated that intraoperative intravenous mannitol administration shows no added value on renal functional preservation after partial nephrectomy (PN) in patients with normal renal function. However, the renoprotective effect of mannitol has not been fully evaluated in patients with preoperative chronic kidney disease (CKD). Materials and Methods: This was a retrospective cohort study with propensity score matching. Patients with a preoperative estimated glomerular filtration rate (eGFR) of <60 mL/minute/1.73 m2 undergoing PN were enrolled in the study between January 2012 and December 2019 in Peking University First Hospital. Participants were divided into two groups: patients who received 25 g of mannitol (group M+) or not (group M-). The primary endpoint was the decreased rate of eGFR at the 6-month follow-up. Results: A total of 244 patients were included in the analysis. After propensity score matching, 80 patients remained in each group. The percentage of decrease from baseline eGFR at postoperative 6-month follow-up showed no difference between the two patient groups (median 11.1 [interquartile range 5.3-25.3] in group M+ vs 12.2 [4.7-21.3] in group M-, median difference -0.7 [95% confidence interval -4.6 to 3.1]; p = 0.704). Postoperative acute kidney injury, renal replacement therapy during hospitalization, postoperative complications, incidence of >20% decrease from baseline eGFR at 6 months, and dialysis at 6 months showed no difference between the two patient groups. Conclusions: A 25 g dose of mannitol administration during PN failed to provide added value on renal functional preservation in CKD patients.

Hyperosmotic stress induces epithelial-mesenchymal transition through rearrangements of focal adhesions in tubular epithelial cells.

Epithelial-mesenchymal transition (EMT) of tubular epithelial cells is a hallmark of renal tubulointerstitial fibrosis and is associated with chronic renal injury as well as acute renal injury. As one of the incidences and risk factors for acute renal injury, increasing the osmolality in the proximal tubular fluid by administration of intravenous mannitol has been reported, but the detailed mechanisms remain unclear. Hyperosmotic conditions caused by mannitol in the tubular tissue may generate not only osmotic but also mechanical stresses, which are known to be able to induce EMT in epithelial cells, thereby contributing to renal injury. Herein, we investigate the effect of hyperosmolarity on EMT in tubular epithelial cells. Normal rat kidney (NRK)-52E cells were exposed to mannitol-induced hyperosmotic stress. Consequently, the hyperosmotic stress led to a reduced expression of the epithelial marker E-cadherin and an enhanced expression of the mesenchymal marker, α-smooth muscle actin (α-SMA), which indicates an initiation of EMT in NKR-52E cells. The hyperosmotic condition also induced time-dependent disassembly and rearrangements of focal adhesions (FAs) concomitant with changes in actin cytoskeleton. Moreover, prevention of FAs rearrangements by cotreatment with Y-27632, a Rho-associated protein kinase inhibitor, could abolish the effects of hyperosmotic mannitol treatment, thus attenuating the expression of α-SMA to the level in nontreated cells. These results suggest that hyperosmotic stress may induce EMT through FAs rearrangement in proximal tubular epithelial cells.

Intravenous Mannitol reduces intracompartmental pressure following tibia fractures: A randomized controlled trial

PurposeImpending compartment syndrome is a common event following closed tibia fractures, which can progress to sinister compartment syndrome. Fasciotomy is the only definitive treatment available, though it has its own drawbacks and complications. Medical management at present consists of limb elevation and adequate hydration. This study aims at determining whether intravenous administration of Mannitol reduced the intracompartmental pressure in patients with closed tibial fractures. MethodsThis is a double blinded, randomized control trial done in a single tertiary care center in India. Forty-five patients were recruited between February 2012 and October 2012. Forty patients who presented to the emergency department with isolated, closed, high velocity, and proximal 2/3 tibia fractures were included in this study. Patients with contraindication to Mannitol were excluded. They were allocated into 2 groups by the investigator using computer generated randomization. The pressure in the anterior compartment of the leg was measured with a handheld Stryker pressure monitor. Then either 20% Mannitol or 0.9% normal saline as given intravenously in a blinded manner, based on the randomization. The intracompartmental pressure was measured at 0, 1 and 3 h after the infusion. The participant, investigator and statistician were masked to the group assessment. ResultsThere was no difference in intracompartmental pressures at 1 or 3 h, between the groups. However, in patients with the baseline of compartmental pressures ≥30 mmHg, Mannitol showed a marked reduction in pressure of 8.5 mmHg at 1 h compared to almost no change in pressure in the saline group. There were no adverse events with the use of Mannitol. ConclusionsThis preliminary study appears to show that Mannitol is useful in the management of the increased compartment pressure. The limitations of this study were that it only involved a small group of patients and the baseline pressures in both the groups were not comparable. More studies are required before the use of Mannitol as a standard of care in the management of compartment syndrome can be established.

Effect of Intravenous Administration of Mannitol on ONSD in Patients With Raised ICP

Effect of Intravenous Administration of Mannitol on ONSD in Patients With Raised ICP

Optical coherence tomography findings in a case of cilioretinal artery occlusion reversal, treated with mannitol and carbogen administration

To present spectral domain optical coherence tomography (OCT) findings during treatment in a case of acute isolated cilioretinal artery occlusion (CLRAO) reversed with intravenous systemic administration of mannitol and carbogen inhalation. Close monitoring with OCT thickness topographic map and cross section scans, every 12 hours, during treatment and till complete reversal of retinal nerve fiber layer edema. Fundus photography and fluorescein angiography (FFA) were used to illustrate occlusion and recanalization. After 72 hours of therapy, visual acuity improved from counting fingers (CF) to 7/10, Snellen’s chart. Consecutively OCT scans showed that the initial macular edema was gradually restored to typical 72 hours of treatment initiation. FFA performed after treatment confirmed recanalization of the cilioretinal artery. Early intervention with the combined intravenous administration of mannitol and carbogen inhalation can reverse acute onset loss of vision due to CLRAO. The reflectivity of retinal layers differs significantly regarding stages of acute CLRAO. In our case report increased reflectivity of the innermost layers of the retina was illustrated and a corresponding reduction in the outer retina and the retinal pigment epithelium and choriocapillaris layers. Macular thickness follow-up data recorded the course of intracellular edema to normal.

Effect of mannitol on globe and orbital volumes in humans.

To determine the effect of intravenous mannitol on globe and orbital volumes. Retrospective chart review of a consecutive series of Cleveland Clinic Neurosurgical Intensive Care Unit patients who underwent computed tomographic imaging before and after intravenous mannitol administration. Volume measurements were performed according to a previously described technique by averaging axial image areas. Measurements before and after mannitol administration were compared using paired t-test. Fourteen patients (28 eyes) met inclusion criteria. Average globe volume decreased 186 mm3 (-2.5%, p = 0.02) after mannitol administration, while average orbital volume increased 353 mm3 (+3.5%, p = 0.04). Average globe volume change for subjects with follow-up scan less than 4.7 hours (mean 1.9 hours; range 0.2-4.5 hours) after mannitol administration was -125 mm3 (-1.7%, p = 0.24) and average orbital volume change was +458 mm3 (+5.1%, p = 0.11). Average globe volume change after mannitol administration for those with follow-up more than 4.7 hours (average 13.9 hours, range 4.9-24.7 hours) was -246 mm3 (-3.3%, p = 0.05) and orbital volume change was +248 mm3 (+2.2%, p = 0.24). Dividing the study population into groups based on mannitol dose did not yield any statistically significant change. Human globe volume decreases after intravenous mannitol administration, while orbital volume increases. These volume changes occur during the time period when intraocular pressure normalizes, after the pressure-lowering effects of the drug. This novel volumetric information improves our understanding of mannitol's mechanism of action and its effects on human ocular and periocular tissues.

Acute angle closure attack after an intravitreal bevacizumab injection for branch retinal vein occlusion: a case report

BackgroundIntravitreal injection is widely used to treat retinal vein occlusion, and acute angle closure (AAC) is an exceptional complication of intravitreal injection. The authors report a case of AAC that occurred immediately after administering intravitreal bevacizumab to treat branch retinal vein occlusion (BRVO).Case presentationA 65-year-old woman was referred to the retina clinic of a tertiary referral center for the treatment of macular edema secondary to BRVO. On slit lamp examination, anterior chamber (AC) depth was shallow (3 corneal thicknesses centrally, 1/4 corneal thicknesses peripherally) in both eyes. Intraocular pressure (IOP) was 19 mmHg in both eyes, and refractive error was +1.00 diopter sphere in both eyes. A gonioscopy exam demonstrated narrow angle of over 180° in both eyes. To treat the macular edema, bevacizumab was injected into her right eye intravitreally. After two bevacizumab injections, the macular edema regressed but recurred 5 months later, and thus, a third injection was performed. The next day, she visited our emergency department complaining of persistent ocular pain in her right eye. The right pupil had dilated to 6 mm diameter and was fixed. Slit lamp exam revealed diffuse corneal edema in her right eye, which had an IOP of 56 mmHg. After administration of intravenous mannitol, the IOP fell to 14 mmHg and the corneal edema disappeared. Subsequently, a glaucoma specialist performed laser iridotomy on the right eye.ConclusionsAlthough AAC is a rare complication of intravitreal injection, it can occur in a patient with risk factors such as hyperopic eye or narrow angle.

Mannitol infusion within 15 min of cross-clamp improves living donor kidney preservation.

BackgroundOptical coherence tomography (OCT) revealed that cells lining proximal convoluted tubules of living donor kidneys (LDKs) procured by laparoscopic procedures were very swollen in response to the brief period of ischemia experienced between the time of arterial vessel clamping and flushing the excised kidney with cold preservation solution. Damage to the tubules as a result of this cell swelling resulted in varying degrees of acute tubular necrosis (ATN) that slowed the recovery of the donor kidneys during the first 2 weeks after their transplantation.MethodsTo prevent this cell damage during LDK procurement, we changed the protocol for intravenous administration of mannitol (i.e., 12.5 or 25 g) to the donor. Specifically, we reduced the time of mannitol administration from 30 to 15 min or less before clamping the renal artery.ResultOCT revealed that this change in the timing of mannitol administration protected the human donor proximal tubules from normothermic-induced cell swelling. An evaluation of posttransplant recovery of renal function showed that patients treated with this modified protocol returned to normal renal function significantly faster than those treated with mannitol 30 min or more before clamping the renal artery.ConclusionBecause slow graft recovery in the first weeks after transplantation represents a risk factor for long-term graft function and survival, we believe that this change in pretreatment protocol will improve renal transplants in patients receiving LDK.

Intracranial haemorrhage with a twist

D. Magnetic resonance venogram. The diagnosis of cerebral venous sinus thrombosis (CVST) was missed preoperatively but suspected intraoperatively when, strikingly, the vein of Labbé was unusually dark, firm and rubbery. Some of the superficial cortical veins were similar in appearance and consistency, and one of these was sent for pathological examination. We traced the vein of Labbé back to the left transverse sinus and suspected it to be thrombosed as well. The brain was swollen and discoloured and the haematoma uneventfully evacuated. MRI venography confirmed the diagnosis of CVST postoperatively (Fig. 1B). A retrospective review of the CT scan on admission revealed left transverse sinus hyperdensity (Fig. 1A). Despite its recognition as a potentially life-threatening clinical entity since 1825,[1]Ameri A. Bousser M.G. Cerebral venous thrombosis.Neurol Clin. 1992; 10: 87-111PubMed Google Scholar CVST remains a diagnostic challenge owing to its protean clinical and radiological presentation.[2]Singh T. Chakera T. Dural sinus thrombosis presenting as unilateral lobar haematomas with mass effect: an easily misdiagnosed cause of cerebral haemorrhage.Australas Radiol. 2002; 46: 351-365Crossref PubMed Scopus (13) Google Scholar CVST accounts for fewer than 2% of patients with non-traumatic intracranial haemorrhage but haemorrhagic transformation of a venous infarct has been reported in 20% to 40% of patients with CVST.3Gum G.K. Numaguchi Y. Foster R.W. et al.Superior sagittal sinus thrombosis with intracerebral hematoma.Comput Radiol. 1987; 11: 199-202Abstract Full Text PDF PubMed Scopus (4) Google Scholar, 4Keiper M.D. Ng S.E. Atlas S.W. et al.Subcortical hemorrhage: marker for radiographically occult cerebral vein thrombosis on CT.J Comput Assist Tomogr. 1995; 19: 527-531Crossref PubMed Scopus (29) Google Scholar While most hemorrhages associated with CVST are small, patchy, or merely petechial foci in larger hypodense areas,1Ameri A. Bousser M.G. Cerebral venous thrombosis.Neurol Clin. 1992; 10: 87-111PubMed Google Scholar, 3Gum G.K. Numaguchi Y. Foster R.W. et al.Superior sagittal sinus thrombosis with intracerebral hematoma.Comput Radiol. 1987; 11: 199-202Abstract Full Text PDF PubMed Scopus (4) Google Scholar, 4Keiper M.D. Ng S.E. Atlas S.W. et al.Subcortical hemorrhage: marker for radiographically occult cerebral vein thrombosis on CT.J Comput Assist Tomogr. 1995; 19: 527-531Crossref PubMed Scopus (29) Google Scholar rapid and dramatic enlargement of lobar hemorrhagic infarction has on rare occasions been observed in the setting of this condition.[5]Stefini R. Latronico N. Cornali C. et al.Emergent decompressive craniectomy in patients with fixed dilated pupils due to cerebral venous and dural sinus thrombosis: report of three cases.Neurosurgery. 1999; 45 (discussion 629-30): 626-629Crossref PubMed Scopus (133) Google Scholar Early diagnosis and expeditious treatment of CVST are essential. This particular patient’s diagnosis was missed on admission and, anecdotally, this appears to be an experience shared more broadly.[2]Singh T. Chakera T. Dural sinus thrombosis presenting as unilateral lobar haematomas with mass effect: an easily misdiagnosed cause of cerebral haemorrhage.Australas Radiol. 2002; 46: 351-365Crossref PubMed Scopus (13) Google Scholar Although the need for aetiological workup and medical treatment via anticoagulation and/or thrombolytic therapy are widely accepted, surgical options also exist for this condition.6Soleau S.W. Schmidt R. Stevens S. et al.Extensive experience with dural sinus thrombosis.Neurosurgery. 2003; 52 (discussion 542-4): 534-544Crossref PubMed Scopus (117) Google Scholar, 7Bentley J.N. Figueroa R.E. Vender J.R. From presentation to follow-up: diagnosis and treatment of cerebral venous thrombosis.Neurosurg Focus. 2009; 27: E4Crossref PubMed Scopus (29) Google Scholar Our patient was found to have protein S deficiency, but other risk factors for CVST are oral contraceptive pill use, pregnancy and oestrogen replacement in females, and underlying malignancies, deficiencies of protein C and factor V Leiden, and vasculitis or anti-phospholipid antibodies.[7]Bentley J.N. Figueroa R.E. Vender J.R. From presentation to follow-up: diagnosis and treatment of cerebral venous thrombosis.Neurosurg Focus. 2009; 27: E4Crossref PubMed Scopus (29) Google Scholar The patient underwent anticoagulation therapy and made an excellent clinical recovery. Intracranial haemorrhage with a twistJournal of Clinical NeuroscienceVol. 19Issue 4PreviewA 55-year-old, previously healthy male train conductor with a history of migraines developed a gradual-onset left temporal headache while at work, followed by new-onset word-finding difficulty. During helicopter transfer from a small regional emergency department to a tertiary referral hospital, the man’s aphasia worsened, and he became densely right hemiplegic and somnolent. After emergent intubation and hyperventilation with concomitant intravenous administration of mannitol, he was taken to the operating room for a definitive procedure. Full-Text PDF

Effect of intravenous mannitol in mobilization of resistant cirrhotic ascites

Cirrhotic ascites is conventionally treated with bed rest, salt restriction, and diuretics. In 20-30% of patients it eventually became resistant to diuretic therapy partly because of reduced sodium excretion owing to the development of resistance against atrial natriuretic peptide. Diuretics resistance can be overcome partially by increasing distal tubular sodium delivery by atrial natriuretic peptide and mannitol administration. To determine the short-term response of intravenous mannitol administration on mobilization of resistant cirrhotic ascites in addition to conventional diuretic treatment. It was an interventional, experimental (double-blind randomized controlled) study conducted in the medical department of Jinnah Hospital, Lahore. A total of 60 patients meeting inclusion and exclusion criteria were included in the study, 30 each in mannitol and placebo groups. Patients were followed for 5 days after the administration with mannitol or placebo. Main outcome measures were increase in 24 h urinary sodium, increase in urinary volume, decrease in weight and abdominal girth. Data showed that all the parameters of response, that is increase in 24 h urinary sodium (cases 34.09±16.71 vs. control 19.16±13.22, P=0.000), increase in urinary volume (cases 260.00±73.58 vs. control 91.67±43.71) decrease in weight (cases 3.07±1.14 vs. control 2.3±1.08, P=0.010) and decrease in abdominal girth (cases 4.70±2.86 vs. control 2.07±1.41, P=0.000) on day 5 of treatment were in favor of mannitol administration. This study shows that resistant ascites can be initially mobilized by infusion of mannitol. The long-term benefits of such therapy are unknown.

Mannitol as salvage treatment for Complex Regional Pain Syndrome Type I

Introduction Complex Regional Pain Syndrome Type I (CRPS I) is a continuation of symptoms and signs due to a pathological exaggerated reaction in an extremity of the human body after an injury or operation. Although the clinical picture of CRPS I in the majority of patients is well known, the underlying pathophysiology remains unclear. In the Netherlands, intravenous mannitol administration used as hydroxyl radical scavenger for patients who do not respond to conservative treatment of CRPS I is advocated but little evidence supports this salvage strategy. In this study the effect of mannitol as salvage medication was evaluated in a well-defined multimodal step-up treatment protocol. Patients and methods A consecutive group of 68 adult patients with persistent CRPS I was analysed, who underwent a total of 100 mannitol infusions. The effect of treatment was considered per sign and per symptom according to the Veldman et al. criteria for CRPS I. Results Overall improvement of CRPS I after mannitol treatment was successful in 24% after 1 week, and in 30% after 1 month. Mannitol treatment had some effect in patients with initially warm CRPS I in contrast to patients with cold CRPS I (OR = 6.30 with CI [2.37–16.75]). Also patients with CRPS I at the upper extremity had more benefit than patients with CRPS I at the lower extremity (OR = 3.26 with CI [1.34–7.93]). Poor results of mannitol treatment were associated with cold CRPS I ( p < 0.001), chronic CRPS I ( p = 0.04) and multiple mannitol treatments ( p = 0.04). Conclusion Mannitol did not significantly contribute to the overall success of treatment in patients with CRPS I. Patients, presenting with acute, warm CRPS I in the upper extremity may have some benefit.

Strategies for handling the insufficiency of the proximal landing zone during endovascular thoracic aortic repair

To discuss two strategies for handling the insufficiency of the proximal landing zone (PLZ) during endovascular thoracic aortic repair. Ten patients underwent endovascular repair (EVR) in the thoracic aorta in one year. Nine patients had DeBakey type III aortic dissection aneurysm (ADA), and one had descending thoracic aortic aneurysm (DTAA). The PLZ, defined as the distance from the origin of the left subclavian artery (LSA) to the primary entry tear of the dissection or the proximal aspect of DTAA, was measured less than 15 mm in all instances by contrast-enhanced CT scan and digital subtraction angiography. The preliminary carotid-carotid and left carotid-subclavian bypass combined with EVR was employed in the DTAA and 3 ADA cases, and the EVR with the intentional coverage of the LSA without the preliminary bypass in the rest 6 ADA patients. The technical success was achieved in all instances. The case of DTAA died of the hemispheric cerebral infarction and subsequent multiple system organ failure, albeit the uneventful recovery from the prior cervical reconstruction. Dizziness occurred in 2 patients (ADA) after the EVR with the intentional bypass-absent coverage of the LSA, but noticeably resolved after the intravenous administration of mannitol for 4 to 5 days. No neurological deficits or limb ischemia developed perioperatively or during the follow-up range from 3 to 12 months. And complete thrombosis of the thoracic aortic false lumen and enlargement of the true lumen were revealed on CT at 3 months in all 9 patients with ADA. Both the adjunctive surgical bypass and the intentional bypass-absent coverage of the left subclavian artery appear feasible in handling the insufficiency of the proximal landing zone during the endovascular thoracic aortic repair. It can expand the EVR applicability in management of DeBakey type III ADAs and DTAAs.

235. The Route of Vector Delivery Impacts the Therapeutic Effects of AAV-Mediated Gene Therapy in Adult Mucopolysaccharidosis IIIB Mice

Mucopolysaccharidosis (MPS) IIIB is an inherited lysosomal storage disease with severe neurological involvement, due to the deficiency of |[alpha]|-N-Acetylglucosaminidase (NaGlu). A critical factor impacting therapeutic development for MPS IIIB is how to efficiently deliver the therapeutic materials into the central nervous system (CNS) to correct the global neurological pathology, which is the cause of high mortality and premature death in MPS IIIB patients. Three delivery strategies, an intravenous (IV) or an intracisternal (IC) injection or combination of an IV and an IC infusion, were considered in studying the therapeutic consequences of adeno-associated viral (AAV) CNS gene delivery in adult MPS IIIB mice. Pretreatment with an IV infusion of mannitol was conducted to facilitate the CNS entry of IV delivered AAV vector and to enhance the dispersion of IC injected vector in the CNS. A therapeutic AAV serotype 2 viral vector (AAV2-CMV-hNaGlu) was used in this study, expressing human NaGlu and controlled by the CMV promoter. Following an IV administration of mannitol, AAV2-CMV-hNaGlu was delivered into young adult MPS IIIB mice by an IV injection (4-8|[times]|1011 viral particles) or by an IC infusion (5|[times]|1010 viral particles), or in combination. In MPS IIIB mice receiving an IV delivery of AAV vector, 20-100% of normal level of NaGlu activity was detected in liver, and the correction of lysosomal storage was observed to be complete in liver and partial in spleen, heart, lung, intestine and skeletal muscle. Intracisternal AAV delivery resulted in a histopathological decrease of lysosomal storage and the expression of functional NaGlu in broad brain areas. No somatic correction of lysosomal storage or detectable NaGlu enzyme activity was observed after IC injection. The therapeutic benefit was also shown by delayed occurrence of neurological symptoms and significantly increased life span in all three treated groups of MPS IIIB mice. The impact of AAV-mediated gene therapy on the life span of MPS IIIB mice was greater in mice treated with a combination of IV and IC delivery (11.1-18.4 months) than by IV (9.2-11.5 months) or IC (10.3-14.0 months) delivery alone, compared with that of non-treated MPS IIIB mice (7.9-11.0 months). In addition, animal behavior studies demonstrated significantly improved activity levels in 31% (5/16) of IV+IC treated MPS IIIB mice, while 48% (13/27) of IV+IC treated mice showed improved performance in a visual cue task. This study demonstrated the great potential of combining IV and IC delivery for improving the AAV CNS gene delivery and developing AAV gene therapy for treating MPS IIIB patients.

Transient keratectasia caused by intraocular pressure elevation after laser in situ keratomileusis

Transient keratectasia developed in association with a marked intraocular pressure (IOP) elevation in a 26-year-old man who had laser in situ keratomileusis (LASIK) for myopia of -9.0 diopters. The keratectasia subsided promptly after the IOP was normalized by an intravenous administration of mannitol. Keratectasia did not recur. Intraocular pressure elevation can cause keratectasia in a structurally compromised cornea after LASIK.

Temporary vessel occlusion for aneurysm surgery: risk factors for stroke in patients protected by induced hypothermia and hypertension and intravenous mannitol administration

Temporary vessel occlusion is an effective technique used by microvascular surgeons to facilitate dissection and permanent clipping of cerebral aneurysms; however, several questions remain regarding the overall safety of this technique. To identify technical and patient-specific risk factors for perioperative stroke, the authors examined a series of patients in whom induced hypertension and mild hypothermia and intravenous mannitol administration were used as protection during temporary vessel occlusion for aneurysm clipping. The study comprises a nonconcurrent prospective analysis of 132 consecutive aneurysm clippings performed with the aid of temporary vascular occlusion and a specific antiischemic anesthetic protocol at the Massachusetts General Hospital from 1991 to 1993. Factors studied included duration of the temporary clip application, number of occlusive episodes, patient age and neurological status, presence of preoperative subarachnoid hemorrhage (SAH), and intraoperative aneurysm rupture ("forced" temporary clipping), as well as whether proximal vessel occlusion or complete aneurysm trapping was used. In a univariate analysis, patient age, intraoperative aneurysm rupture, temporary clipping lasting more than 20 minutes, clipping between the 4th and 10th day after SAH, and multiple clipping episodes were all significantly associated with stroke outcome. Multivariate logistic regression revealed that intraoperative aneurysm rupture (relative risk 5.6, p = 0.02) and a duration of temporary clip application that lasted more than 20 minutes (relative risk 9.4, p = 0.04) were independently associated with stroke outcome. Overall, 5.2% of the patients had postoperative clinical strokes. Based on their findings the authors conclude that temporary clipping is a safe adjunct to aneurysm surgery, particularly when the duration of clipping is short.

The effect of mannitol on intracranial pressure in relation to serum osmolality in a cat model of cerebral edema.

To determine whether intravenous mannitol administration reduces intracranial pressure (ICP) in a cat model of brain edema by changing serum osmolality. Prospective, controlled study. Pediatric intensive care unit laboratory in a university hospital. Intraparenchymal ICP monitors were placed in 12 adult cats which subsequently underwent 60 min of continuous arteriovenous hemofiltration with countercurrent dialysis (CAVH-D), using sterile water with potassium chloride as a dialysate. The ultrafiltrate was replaced with a hypotonic solution causing a rapid reduction in serum osmolality while maintaining a euvolemic state. In six cats (control group) no further interventions were instituted, while in the six other cats (mannitol group) 1g/kg mannitol was administered intravenously immediately after CAVH-D had been discontinued. ICP was monitored continuously, and serum osmolality was determined at 15-min intervals during CAVH-D and for 30 min thereafter. ICP increased significantly in both the control and mannitol groups during 60 min of CAVH-D. After CAVH-D, ICP was reduced in the mannitol group while ICP remained significantly higher in the control group. An inverse linear correlation was demonstrated between serum osmolality and ICP values in the control group throughout the experiment, as well as during the first 60 min in the mannitol group. However, no such correlation existed in the mannitol group after mannitol administration, as no significant changes in serum osmolality were observed while a marked reduction in ICP values occurred. Mannitol is effective in reducing increased ICP in this model of euvolemic brain edema. However, 15 min after mannitol administration, no relationship between a continued decrease in ICP and a change in serum osmolality could be established. We postulate that the beneficial effect on ICP by mannitol outlasts its possible instantaneous and short-lived effect on serum osmolality.

Ciguatera: Current concepts

Ciguatera poisoning develops after ingestion of certain coral reef-associated fish. With travel to and from the tropics and importation of tropical food fish increasing, ciguatera has begun to appear in temperate countries with more frequency. The causative agents are certain varieties of the protozoan dinoflagellate Gambierdiscus toxicus, but bacteria associated with these protozoa may have a role in toxin elaboration. A specific "ciguatoxin" seems to cause the symptoms, but toxicosis may also be a result of a family of toxins. Toxicosis develops from 10 minutes to 30 hours after ingestion of poisoned fish, and the syndrome can include gastrointestinal and neurologic symptoms, as well as chills, sweating, pruritus, bradycardia, tachycardia, and long-lasting weakness and fatigue. More severe features are rare. In this review, the pathophysiologic features and symptoms of ciguatera are reviewed and compared with those of other seafood-related syndromes. Although no definitive therapy is known, the most promising treatment for ciguatera is intravenous administration of mannitol. Physicians should warn patients who are traveling to endemic areas about this toxicosis.

Mannitol, Intracranial Pressure, and Vasogenic Edema

The effect of a 2 g/kg intravenous bolus of mannitol on intracranial pressure (ICP) and white matter water content was determined by following the time course of ICP and spatial white matter water content after administration of mannitol in a hemispheric cold lesion model of vasogenic edema in the cat. After mannitol infusion, maximal ICP reduction occurred at approximately 20 minutes and began to return to baseline after 26 minutes. White matter water content in the control hemisphere began to decrease much later, reaching a minimum at 60 minutes. White matter water content in the lesioned hemisphere was not changed significantly after mannitol infusion. We conclude that the rapid reduction of ICP after intravenous administration of mannitol is not solely due to the dehydration of white matter.

Mannitol, Intracranial Pressure, and Vasogenic Edema

The effect of a 2 g/kg intravenous bolus of mannitol on intracranial pressure (ICP) and white matter water content was determined by following the time course of ICP and spatial white matter water content after administration of mannitol in a hemispheric cold lesion model of vasogenic edema in the cat. After mannitol infusion, maximal ICP reduction occurred at approximately 20 minutes and began to return to baseline after 26 minutes. White matter water content in the control hemisphere began to decrease much later, reaching a minimum at 60 minutes. White matter water content in the lesioned hemisphere was not changed significantly after mannitol infusion. We conclude that the rapid reduction of ICP after intravenous administration of mannitol is not solely due to the dehydration of white matter.