scholarly journals Delayed-onset white cord syndrome after anterior and posterior cervical decompression surgery for symptomatic ossification of spinal ligaments: illustrative cases

2021 ◽  
Vol 1 (19) ◽  
Author(s):  
Ranjit D. Singh ◽  
Mark P. Arts ◽  
Godard C. W. de Ruiter
Keyword(s):  
Mean Arterial Pressure ◽  
Physical Therapy ◽  
Arterial Pressure ◽  
Rare Complication ◽  
Decompressive Surgery ◽  
Neurological Deficits ◽  
High Dose ◽  
Decompression Surgery ◽  
Hyperintense Signal ◽  
Early Physical Therapy

BACKGROUND White cord syndrome is an extremely rare complication of cervical decompressive surgery, characterized by serious postoperative neurological deficits in the absence of apparent surgical complications. It is named after the characteristic ischemic-edematous intramedullary T2-hyperintense signal on postoperative magnetic resonance imaging and is believed to be caused by ischemic-reperfusion injury. Neurological deficits typically manifest immediately after surgery, and delayed occurrence has been reported only once. OBSERVATIONS The authors presented two cases of delayed white cord syndrome after anterior and posterior cervical decompression surgery for symptomatic ossification of the posterior longitudinal ligament and ligamentum flavum, respectively. Neurological deficits manifested on postoperative day 2 (case 1) and day 8 (case 2). The patients’ conditions were managed with high-dose corticosteroids, mean arterial pressure augmentation, and early physical therapy, after which they showed partial neurological recovery at discharge, which improved further by the 3-month follow-up visit. LESSONS The authors’ aim was to raise awareness among spine surgeons about this rare but severe complication of cervical decompressive surgery and to emphasize the mainstays of treatment based on current best evidence: high-dose corticosteroids, mean arterial pressure augmentation, and early physical therapy.

Effects of Ambulation and Nondependent Transfers on Vital Signs in Patients Receiving Norepinephrine

2017 ◽  
Vol 26 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Rosario Arcaya Nievera ◽  
Ann Fick ◽  
Hilary K. Harris
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Physical Therapy ◽  
Arterial Pressure ◽  
Low Dose ◽  
Vital Signs ◽  
Activity Level ◽  
Significant Difference ◽  
Before And After ◽  
Norepinephrine Dose

Purpose To assess the safety of mobilizing patients receiving low-dose norepinephrine (0.05 μg/kg per min) by examining mean arterial pressure and heart rate before and after activity with parameters set by the physician. Background Norepinephrine is a peripheral vasoconstrictor administered for acute hypotension. During activity, blood flows to the periphery to supply muscles with oxygen, which may oppose the norepinephrine vasoconstriction. The safety of mobilizing patients receiving norepinephrine is unclear. Methods Heart rate, mean arterial pressure, norepinephrine dose, and activity performed were extracted retrospectively from charts of 47 cardiothoracic surgery patients during the first patient transfer to chair or ambulation with norepinephrine infusing. Mean arterial pressure and heart rate were compared before and after physical therapy (paired t tests). Differences among norepinephrine doses and physical activity levels were evaluated (Kruskal-Wallis test). Results Forty-one of the 47 patients (87%) tolerated the activity within safe ranges of vital signs. The change in patients’ mean arterial pressure from before to after activity was not significant (P = .16), but a significant increase in heart rate occurred after activity (P < .001). A Kruskal-Wallis test showed no significant difference in the norepinephrine dose and activity level (χ2 = 6.34, P = .17). No instances of cardiopulmonary or respiratory arrest occurred during any physical therapy sessions. Conclusions Infusion of low-dose norepinephrine should not be considered an automatic reason to keep patients on bed rest.

POLYTETRAFLUOROETHYLENE-INDUCED GRANULOMA AND BRAINSTEM CYST AFTER MICROVASCULAR DECOMPRESSION FOR TRIGEMINAL NEURALGIA

Neurosurgery ◽  
2007 ◽  
Vol 61 (4) ◽  
pp. E875-E877 ◽  
Author(s):  
Gabor Toth ◽  
Helene Rubeiz ◽  
R. Loch Macdonald
Keyword(s):  
Trigeminal Neuralgia ◽  
Microvascular Decompression ◽  
Clinical Presentation ◽  
Rare Complication ◽  
Granulomatous Inflammation ◽  
Neurological Deficits ◽  
Decompression Surgery ◽  
Idiosyncratic Reaction ◽  
First Case ◽  
Microvascular Decompression Surgery

Abstract OBJECTIVE Microvascular decompression is commonly performed for medically refractory trigeminal neuralgia. A piece of polytetrafluoroethylene (PTFE) is usually placed between the trigeminal nerve and the blood vessel causing the compression. The procedure is effective and relatively safe, and PTFE is presumed to be inert. Reactions to PTFE are rare. CLINICAL PRESENTATION We report a patient who developed progressive neurological symptoms 5 years after microvascular decompression surgery. Imaging showed an enhancing cerebellopontine mass resembling a posterior fossa tumor with a large cyst compressing the brainstem. INTERVENTION Craniotomy was performed to decompress the cyst. Biopsy of the enhancing mass showed granulomatous inflammation. The patient underwent a second brainstem decompression surgery with placement of a catheter in the cyst connected to an Ommaya reservoir; she has moderate to severe residual neurological deficits. CONCLUSION This may be the first case of a severely disabling, space-occupying cyst resulting from a reaction to intracranial PTFE. Should this exceptionally rare complication be disclosed to patients or is it an idiosyncratic reaction unlikely to occur again?

scholarly journals N omega-amino-L-arginine, an inhibitor of nitric oxide synthase, raises vascular resistance but increases mortality rates in awake canines challenged with endotoxin.

1992 ◽  
Vol 176 (4) ◽  
pp. 1175-1182 ◽  
Author(s):  
J P Cobb ◽  
C Natanson ◽  
W D Hoffman ◽  
R F Lodato ◽  
S Banks ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Septic Shock ◽  
Mean Arterial Pressure ◽  
Nitric Oxide Synthase ◽  
Animal Models ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Mortality Rates ◽  
High Dose ◽  
Oxide Synthase

Inhibitors of nitric oxide synthase (NOS) have been reported to increase mean arterial pressure in animal models of sepsis and recently have been given to patients in septic shock. However, controlled studies to determine the effects of these agents on cardiovascular function and survival in awake animal models of sepsis have not been reported. To examine the therapeutic potential of NOS inhibition in septic shock, we challenged canines with endotoxin (2 or 4 mg/kg i.v.) and treated them with either normal saline or N omega-amino-L-arginine (10 or 1 mg/kg/h), the most specific inhibitor available for the isoform of NOS implicated in septic shock. Endotoxemic animals treated with N omega-amino-L-arginine (n = 11) had higher systemic and pulmonary vascular resistance indices (SVRI and PVRI, p less than or equal to 0.033) and decreased heart rates (p = 0.009), cardiac indices (CI, p = 0.01), oxygen delivery indices (p = 0.027), and oxygen consumption indices (p = 0.046) compared with controls (n = 6). Moreover, N omega-amino-L-arginine increased mortality rates after endotoxin challenge (10 of 11 vs. 1 of 6 controls, p = 0.005). Administration of L-arginine did not improve survival or alter the cardiopulmonary effects of N omega-amino-L-arginine, which suggests that inhibition of NOS may not have been competitive. In normal animals, N omega-amino-L-arginine alone (n = 3) increased SVRI (p = 0.0008) and mean arterial pressure (p = 0.016), and decreased CI (p = 0.01) compared with saline-treated controls (n = 3), but, at the high dose, also produced neuromuscular rigidity and seizure-like activity that was not apparent in the endotoxemic model. Thus, the mortality rate from endotoxemia increased either because of NOS inhibition per se or because of properties unique to N omega-amino-L-arginine, or both.

Effects of aging on cerebral vascular responses to serotonin in rats

1993 ◽  
Vol 264 (6) ◽  
pp. H2136-H2140 ◽  
Author(s):  
M. A. Hajdu ◽  
R. T. McElmurry ◽  
D. D. Heistad ◽  
G. L. Baumbach
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Low Dose ◽  
Cerebral Arteries ◽  
High Dose ◽  
Aged Rats ◽  
Adult Rats ◽  
Effects Of Aging

The purpose of this study was to examine effects of aging on responses of large cerebral arteries to serotonin. We measured cerebral microvascular pressure (with a micropipette and servo-null method), diameter of pial arterioles, and cerebral blood flow (microspheres) in adult (12- to 14-mo-old, n = 15) and aged (24- to 27-mo-old, n = 14) Wistar rats. Responses to intra-atrial infusion of serotonin (5 and 50 micrograms.kg-1.min-1) were examined. Infusion of the low dose of serotonin decreased mean arterial pressure and pial arteriolar pressure in adult and aged rats to similar levels. Cerebral blood flow was not reduced in adult or aged rats during infusion of the low dose of serotonin. The high dose of serotonin did not affect mean arterial pressure but reduced pial arteriolar pressure [from 46 +/- 4 to 23 +/- 2 (SE) in adult rats and from 52 +/- 3 to 18 +/- 4 mmHg in aged rats]. The high dose of serotonin increased large-artery resistance from 0.9 +/- 0.1 to 1.6 +/- 0.2 in adult rats and from 0.9 +/- 0.1 to 2.7 +/- 0.6 mmHg.ml-1.min.100 g in aged rats. Cerebral blood flow was reduced significantly in aged rats (from 59 +/- 3 to 41 +/- 6 ml.min-1.100 g-1), but not in adult rats, during infusion of the high dose of serotonin. We conclude that aging augments constrictor responses of large cerebral arteries to intravascular serotonin, which results in a reduction of cerebral blood flow in aged but not adult rats.

Hypertension induced by blockade of ETB receptors in conscious nonhuman primates: role of ETAreceptors

2002 ◽  
Vol 283 (4) ◽  
pp. H1555-H1561 ◽  
Author(s):  
Glenn A. Reinhart ◽  
Lee C. Preusser ◽  
Sandra E. Burke ◽  
Jerry L. Wessale ◽  
Craig D. Wegner ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Nonhuman Primates ◽  
High Dose ◽  
Cynomolgus Monkeys ◽  
Selective Antagonist ◽  
Sustained Hypertension ◽  
Endothelin B

The role of endothelin-B (ETB) receptors in circulatory homeostasis is ambiguous, reflecting vasodilator and constrictor effects ascribed to the receptor and diuretic and natriuretic responses that could oppose the hypertensive effects of ET excess. With the use of conscious, telemetry-instrumented cynomolgus monkeys, we characterized the hypertension produced by ETB blockade and the role of ETA receptors in mediating this response. Mean arterial pressure (MAP) and heart rate (HR) were measured 24 h/day for 24 days under control conditions and during administration of the ETB-selective antagonist A-192621 (0.1, 1.0, and 10 mg/kg bid, 4 days/dose) followed by coadministration of the ETAantagonist atrasentan (5 mg/kg bid) + A-192621 (10 mg/kg bid) for another 4 days. High-dose ETB blockade increased MAP from 79 ± 3 (control) to 87 ± 3 and 89 ± 3 mmHg on the first and fourth day, respectively; HR was unchanged, and plasma ET-1 concentration increased from 2.1 ± 0.3 pg/ml (control) to 7.24 ± 0.99 and 11.03 ± 2.37 pg/ml. Atrasentan + A-192621 (10 mg/kg) decreased MAP from hypertensive levels (89 ± 3) to 75 ± 2 and 71 ± 4 mmHg on the first and fourth day, respectively; plasma ET-1 and HR increased to 26.64 ± 3.72 and 28.65 ± 2.89 pg/ml and 113 ± 5 (control) to 132 ± 5 and 133 ± 7 beats/min. Thus systemic ETB blockade produces a sustained hypertension in conscious nonhuman primates, which is mediated by ETA receptors. These data suggest an importance clearance function for ETB receptors, one that influences arterial pressure homeostasis indirectly by reducing plasma ET-1 levels and minimizing ETA activation.

scholarly journals Activation of spinal opioid receptors contributes to hypotension after hemorrhage in conscious rats

1999 ◽  
Vol 276 (5) ◽  
pp. H1552-H1558 ◽  
Author(s):  
Kooi K. Ang ◽  
Robert J. McRitchie ◽  
Jane B. Minson ◽  
Ida J. Llewellyn-Smith ◽  
Paul M. Pilowsky ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Opioid Receptors ◽  
High Dose ◽  
Binding Affinities ◽  
Opioid Antagonists ◽  
Severe Hemorrhage ◽  
Effective Doses ◽  
Spinal Opioid

Opioid receptors are activated during severe hemorrhage, resulting in sympathoinhibition and a profound fall in blood pressure. This study examined the location and subtypes of opioid receptors that might contribute to hypotension after hemorrhage. Intrathecal naloxone methiodide (100 nmol) abolished the fall in blood pressure after hemorrhage (1.5% of body wt; mean arterial pressure 122 ± 8 mmHg after naloxone methiodide vs. 46 ± 5 mmHg in controls, P < 0.001). Intracisternal naloxone methiodide was less effective than intrathecal naloxone methiodide, whereas intravenous naloxone methiodide, which does not cross the blood-brain barrier, did not alter the fall in blood pressure after hemorrhage. These results demonstrate that spinal opioid receptors contribute to hypotension after hemorrhage but do not exclude supraspinal effects. In separate experiments, the subtype-specific opioid antagonists ICI-174864 (δ-antagonist), norbinaltorphimine (nor-BNI; κ-antagonist), and H-d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH2(CTOP; μ-antagonist) were each administered intrathecally to determine the minimum dose that would attenuate hypotension during severe hemorrhage. These antagonists were effective at similar doses (3 nmol for CTOP, 6 nmol for ICI-174864, and 10 nmol for nor-BNI), although the binding affinities of these three different agents for their target receptors varied >1600-fold. Comparisons of the minimum effective doses of these antagonists in relation to their binding affinities provides strong evidence for the participation of δ-receptors in mediating hypotension after hemorrhage. In contrast, the dose at which nor-BNI was effective suggests an effect at δ-receptors but not κ-receptors. The efficacy of CTOP, albeit at a high dose, also suggests an effect at μ-receptors.

scholarly journals Insulin versus Lipid Emulsion in a Rabbit Model of Severe Propranolol Toxicity: A Pilot Study

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Martyn Harvey ◽  
Grant Cave ◽  
Daniel Lahner ◽  
Jan Desmet ◽  
Gaynor Prince ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Beta Blocker ◽  
Lipid Emulsion ◽  
Rabbit Model ◽  
Rate Pressure Product ◽  
High Dose ◽  
Mechanically Ventilated ◽  
Proximal Small Bowel

Background and objective. Beta-blocker overdose may result in intractable cardiovascular collapse despite conventional antidotal treatments. High dose insulin/glucose (ING), and more recently intravenous lipid emulsion (ILE), have been proposed as potentially beneficial therapies in beta blocker intoxication. We compare efficacy of the novel antidotes ING, with ILE, in a rabbit model of combined enteric/intravenous propranolol toxicity.Methods. Sedated, mechanically ventilated and invasively monitored New Zealand White rabbits underwent mini-laparotomy and enterostomy formation with 40 mg/kg propranolol instilled into the proximal small bowel. At 30 minutes propranolol infusion was commenced at 4 mg/kg/hr and continued to a target mean arterial pressure (MAP) of 50% baseline MAP. Animals were resuscitated with insulin at 3 U/kg plus 0.5 g/kg glucose (ING group), or 10 mL/kg 20% Intralipid (ILE group).Results. Rate pressure product (RPP; RPP = heart rate × mean arterial pressure) was greatest in the ING group at 60 minutes (P<.05). A trend toward greater heart rate was observed in the ING group (P=.06). No difference was observed in survival between groups (4/5 ING versus 2/5 ILE;P=.524).Conclusions. High dose insulin resulted in greater rate pressure product compared with lipid emulsion in this rabbit model of severe enteric/intravenous propranolol toxicity.

scholarly journals MON-239 Pituitary Apoplexy Induced by Gonadotropin-Releasing Hormone Agonist Administration: A Rare Complication of Prostate Cancer Treatment

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mariana Marques Barbosa ◽  
Sílvia Cristina de Sousa Paredes ◽  
Maria João Machado ◽  
Rui Almeida ◽  
Olinda Castro Marques
Keyword(s):  
Prostate Cancer ◽  
Gnrh Agonist ◽  
Pituitary Apoplexy ◽  
Rare Complication ◽  
Gonadotropin Releasing Hormone ◽  
Department Head ◽  
Total Testosterone ◽  
High Dose ◽  
Releasing Hormone ◽  
Hyperintense Signal

Abstract Background: Pituitary apoplexy is a potentially life-threatening clinical condition associated with bleeding and/or infarction into the pituitary gland, usually within a tumor. Gonadotropin-releasing hormone (GnRH) agonists, currently used in the treatment of advanced prostate cancer, have been described in the literature as a rare cause of pituitary apoplexy. Case: We report the case of a 69 year-old man with a known pituitary macroadenoma incidentally detected in 2016, without further investigation. He was diagnosed with prostate cancer in 2017 and underwent retropubic prostatectomy. Two years later there was evidence of histologic prostate tumor progression, so he started treatment with leuprorelin 45mg (GnRH agonist). Immediately after the first subcutaneous injection he presented with acute-onset severe headache, followed by left eye ptosis, diplopia and vomiting. Left cranial nerve III palsy was confirmed by examination in the emergency department. Head computed tomography showed a lesion in the sellar region; laboratory endocrine workup was significant for total testosterone 72.07 ng/dL (86.49 – 788.22), with no other abnormalities. Magnetic resonance imaging of the pituitary revealed tumor enlargement and a T1-hyperintense signal, compatible with recent haemorrhagic sellar content. The patient was managed conservatively with high dose steroids, and symptoms were significantly improved on discharge. Discussion: Pituitary apoplexy induced by GnRH agonist administration is a rare complication, described in only 20 documented cases to date. The pathophysiologic mechanism involved is not clearly established and several hypotheses have been proposed: a combination of metabolic hyperactivity, cell division/tumor growth and increased intrasellar pressure, inducing ischemia in a poorly perfused adenomatous tissue given the demand. Although uncommon, healthcare professionals should be aware of this serious consequence of GnRH agonist administration and recognize the signs, preventing a delay in diagnosis and treatment.

scholarly journals Norepinephrine potentiates the efficacy of volume expansion on mean systemic pressure in septic shock

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Imane Adda ◽  
Christopher Lai ◽  
Jean-Louis Teboul ◽  
Laurent Guerin ◽  
Francesco Gavelli ◽  
...  
Keyword(s):  
Septic Shock ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Low Dose ◽  
Haemodynamic Effect ◽  
High Dose ◽  
Systemic Pressure ◽  
Preload Responsiveness ◽  
Mean Systemic Pressure

Abstract Background Through venous contraction, norepinephrine (NE) increases stressed blood volume and mean systemic pressure (Pms) and exerts a “fluid-like” effect. When both fluid and NE are administered, Pms may not only result from the sum of the effects of both drugs. Indeed, norepinephrine may enhance the effects of volume expansion: because fluid dilutes into a more constricted, smaller, venous network, fluid may increase Pms to a larger extent at a higher than at a lower dose of NE. We tested this hypothesis, by mimicking the effects of fluid by passive leg raising (PLR). Methods In 30 septic shock patients, norepinephrine was decreased to reach a predefined target of mean arterial pressure (65–70 mmHg by default, 80–85 mmHg in previously hypertensive patients). We measured the PLR-induced increase in Pms (heart–lung interactions method) under high and low doses of norepinephrine. Preload responsiveness was defined by a PLR-induced increase in cardiac index ≥ 10%. Results Norepinephrine was decreased from 0.32 [0.18–0.62] to 0.26 [0.13–0.50] µg/kg/min (p < 0.0001). This significantly decreased the mean arterial pressure by 10 [7–20]% and Pms by 9 [4–19]%. The increase in Pms (∆Pms) induced by PLR was 13 [9–19]% at the higher dose of norepinephrine and 11 [6–16]% at the lower dose (p < 0.0001). Pms reached during PLR at the high dose of NE was higher than expected by the sum of Pms at baseline at low dose, ∆Pms induced by changing the norepinephrine dose and ∆Pms induced by PLR at low dose of NE (35.6 [11.2] mmHg vs. 33.6 [10.9] mmHg, respectively, p < 0.01). The number of preload responders was 8 (27%) at the high dose of NE and 15 (50%) at the low dose. Conclusions Norepinephrine enhances the Pms increase induced by PLR. These results suggest that a bolus of fluid of the same volume has a greater haemodynamic effect at a high dose than at a low dose of norepinephrine during septic shock.

How we significantly reduced oesophagectomy leaks and the significance of Mean Arterial Pressure

2017 ◽  
Author(s):  
C Reissfelder ◽  
T Mees ◽  
S Schölch ◽  
A Remer ◽  
A Seifert ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure
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