Archive for August 19th, 2008

Trauma Death & Dying

by Paul Rega, MD — published on August 19th, 2008

Jacobs LM et al. “Trauma Death: Views of the Public and Trauma Professionals on Death and Dying From Injuries” Arch Surg 2008; 143(8): 730-735.

ABSTRACT

Objectives  To determine the values and preferences of the general public and trauma professionals regarding end-of-life care due to injury so as to inform practice guidelines.

Design, Setting, and Participants  Surveys of the general public sampled by random-digit dialing between June 6, 2005, and July 5, 2005, and of a convenience sample of trauma professionals during fall 2005 in the United States were conducted regarding preferences for care in the prehospital, emergency, and critical care settings.

Main Outcome Measures  Responses to the survey questions.

Results  Most of the public and trauma professionals would prefer palliative care when doctors determine that aggressive critical care would not be beneficial in saving their lives. During resuscitation of an injured loved one, 51.9% of the public and 62.7% of the professionals would prefer to be in the emergency department treatment room. Most of the public believes that patients should have the right to demand care not recommended by their physicians. Most of both groups trust a doctor’s decision to withdraw treatment when futility is determined. More of the public (57.4%) than the professionals (19.5%) believe that divine intervention could save a person when physicians believe treatment is futile. Other findings suggest further important insights.

Conclusions  The results pose challenges that will require societal discourse to determine the best practice. Resolutions will need to be included in educational curricula and incorporated into practice to ensure that dying trauma victims and their families receive quality end-of-life care.

Further findings (http://www.medpagetoday.com/EmergencyMedicine/EmergencyMedicine/tb/10582):

 

  • The rate of emergency care is not much different among the public or professionals — 46.2% of the public and 47.4% of trauma professionals had received emergency treatment in the previous decade.
  • More than half (51.9%) of the public and 62.7% of professionals said they would like to be in the emergency department treatment area while an injured loved one was resuscitated.
  • Nearly three-quarters of the public — 72.4% — believe trauma patients have a right to demand care not deemed appropriate by a physician, compared with only 44.3% of professionals.
  • On the other hand, most of both groups said they would trust a physician’s decision to withdraw treatment when it would be futile. On a one-to-10 scale, where one is no trust and 10 is complete trust, the average score among the public was 7.0, compared with 9.4 among trauma professionals.
  • Professionals were more likely to have signed organ donor cards than the general public, at 78.9% versus 50.6%.
  • When making decisions about their own medical care, religious beliefs would be important to 41% of the public and 30.6% of professionals.
  • At the same time, 61.3% of the public and 20.2% of professionals believe that a miracle can a save person in a persistent vegetative state, and 57.4% of the public said divine intervention can save a person when doctors think treatment is futile, compared with just 19.5% of trauma professionals.

 

Interestingly, on the tough question of when to stop life-sustaining treatment, 72.8% of the public and 92.6% of professionals think if there’s no hope for recovery, the focus of care should shift to the comfort of the dying patients.

 

But among the minority who disagreed, 86.2% of the public and 33.3% of the professionals said treatment aimed at recovery should continue regardless of cost. On the other hand, when such aggressive care meant taking resources away from those with a better chance of life, members of the minority changed their minds — 56.1% of the public and 62.8% of the professionals said the care should cease.
 

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categories: Emergency Medicine

Age bias in trauma?

by Paul Rega, MD — published on August 19th, 2008

Chang D, et al “Undertriage of elderly trauma patients to state-designated trauma centers” Arch Surg 2008; 143: 776-781.
Objective  To determine whether age bias is a factor in triage errors.

Design  Retrospective analysis of 10 years (1995-2004) of prospectively collected data in the statewide Maryland Ambulance Information System followed by surveys of emergency medical services (EMS) and trauma center personnel at regional EMS conferences and level I trauma centers, respectively.

Patients  Trauma patients were defined as those who met American College of Surgeons physiology, injury, and/or mechanism criteria and were subjectively declared priority I status by EMS personnel.

Main Outcome Measure  Undertriage, defined as when trauma patients were not transported to a state-designated trauma center.

Results  The registry analysis identified 26 565 trauma patients. The undertriage rate was significantly higher in patients aged 65 years or older than in younger patients (49.9% vs 17.8%, P < .001). On multivariate analysis, this decrease in trauma center transports was found to start at age 50 years (odds ratio, 0.67; 95% confidence interval, 0.57-0.77), with another decrease at age 70 years (odds ratio, 0.45; 95% confidence interval, 0.39-0.53) compared with patients younger than 50 years. A total of 166 respondents participated in the follow-up surveys and ranked the top 3 causal factors for this undertriage as inadequate training, unfamiliarity with protocol, and possible age bias.

Conclusions  Even when trauma is recognized and acknowledged by EMS, providers are consistently less likely to consider transporting elderly patients to a trauma center. Unconscious age bias, in both EMS in the field and receiving trauma center personnel, was identified as a possible cause.

 

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categories: Emergency Medicine

Intraarticular Lidocaine & Dislocated Shoulder

by Paul Rega, MD — published on August 19th, 2008

Academic Emergency Medicine

Volume 15 Issue 8, Pages 703 - 708

Intraarticular Lidocaine versus Intravenous Procedural Sedation with Narcotics and Benzodiazepines for Reduction of the Dislocated Shoulder: A Systematic Review
Robert Warne Fitch, MD, John E. Kuhn, MD

From Vanderbilt Sports Medicine (RWF, JEK), Nashville, TN.

ABSTRACT

Background: Anterior shoulder dislocations commonly present to the emergency department (ED). The time associated with procedural sedation for the reduction of anterior shoulder dislocations can be lengthy and may require use of additional personnel. Complications associated with intravenous (IV) medications for procedural sedation are well documented.

Objectives: The aim was to determine if intraarticular lidocaine (IAL) injection is as effective as IV procedural sedation with narcotics and benzodiazepines for reduction of anterior shoulder dislocations.

Methods: This was a systematic review of randomized controlled trials (RCTs). The authors performed a PubMed, EMBASE, and Cochrane database search using key words: “shoulder dislocation” and “reduction” and retrieved every RCT published that compared the use of IV sedation to IAL as medication for reduction. Each manuscript was reviewed and the results of each was compared regarding medications used, success of reduction, complications, pain perceived, ease of reduction, and time spent in the ED.

Results: Six Level 1 RCTs were identified. No studies showed a statistically significant difference in success rate between IAL versus IV sedation. The complication rate was significantly higher in the IV sedation groups (p < 0.001), and the total time spent in the ED was longer for the IV sedation group.

Conclusions: The use of IAL for reduction of anterior shoulder dislocations should be strongly considered as a first line therapy because it is effective and safe and may potentially reduce time spent in the ED.

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categories: Emergency Medicine

Noninvasive Ventilation in CHF

by Paul Rega, MD — published on August 19th, 2008

Academic Emergency Medicine

Volume 15 Issue 4, Pages 355 - 362

Published Online: 29 Feb 2008

Noninvasive Ventilation Outcomes in 2,430 Acute Decompensated Heart Failure Patients: An ADHERE Registry Analysis
Thomas A. Tallman, DO, W. Frank Peacock, MD, Charles L. Emerman, et al. 

 

ACADEMIC EMERGENCY MEDICINE 2008; 15:355–362 © 2008 by the Society for Academic Emergency Medicine

ABSTRACT

Objectives: Continuous or bilevel positive airway pressure ventilation, called noninvasive ventilation (NIV), is a controversial therapy for acute decompensated heart failure (ADHF). While NIV is considered safe and effective in patients with chronic obstructive pulmonary disease (COPD), clinical trial data that have addressed safety in ADHF patients are limited, with some suggestion of increased mortality. The objective of this study was to assess mortality outcomes associated with NIV and to determine if a failed trial of NIV followed by endotracheal intubation (ETI) (NIV failure) is associated with worse outcomes, compared to immediate ETI.

Methods: This was a retrospective analysis of the Acute Decompensated Heart Failure National Registry (ADHERE), which enrolls patients with treatment for, or with a primary discharge diagnosis of, ADHF. The authors compared characteristics and outcomes in four groups: no ventilation, NIV success, NIV failure, and ETI. One-way analysis of variance or Wilcoxon testing was performed for continuous data, and chi-square tests were used for categorical data. In addition, multivariable logistic regression was used to adjust mortality comparisons for risk factors.

Results: Entry criteria were met by 37,372 patients, of which 2,430 had ventilation assistance. Of the ventilation group, 1,688 (69.5%) were deemed NIV success, 72 (3.0%) were NIV failures, and 670 (27.6%) required ETI. The NIV failure group had the lowest O2 saturation (SaO2) (84 ± 16%), compared to either NIV success (89.6 ± 10%) or ETI (88 ± 13%; p = 0.017). ETI patients were more likely to receive vasoactive medications (p < 0.001) than the NIV success cohort. When comparing NIV failures to ETI, there were no differences in treatment during hospitalization (p > 0.05); other than that the NIV failure group more often received vasodilators (68.1% vs. 54.3%; p = 0.026). In-hospital mortality was 7.9% with NIV, 13.9% with NIV failure, and 15.4% with ETI. After risk adjustment, the mortality odds ratio for NIV failure versus ETI increased to 1.43, although this endpoint was not statistically significant.

Conclusions: In this analysis of ADHF patients receiving NIV to date, patients placed on NIV for ADHF fared better than patients requiring immediate ETI. Patients who failed NIV and required ETI still experienced lower mortality than those initially placed on ETI. Thus, while the ETI group may be more severely ill, starting therapy with NIV instead of immediate ETI will likely not harm the patient. When ETI is required, mortality and length of stay may be adversely affected. Since a successful trial of NIV is associated with improved outcomes in patients with ADHF, application of this therapy may be a reasonable treatment option.

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categories: Emergency Medicine

Intubating the Obese

by Paul Rega, MD — published on August 19th, 2008
The Impact of Obesity on the Outcome of Emergency Intubation in Trauma Patients.

Original Articles

Journal of Trauma-Injury Infection & Critical Care. 65(2):396-400, August 2008.
Sifri, Ziad C. MD; Kim, Hyonah MD; Lavery, Rob MA; Mohr, Alicia MD; Livingston, David H. MD

Abstract:
Objective: Emergency intubation of trauma patients is a complex intervention, which can be safely and successfully performed in most trauma centers. This, however, has never been validated in the obese trauma population. Obese patients have anatomic and physiologic characteristics that make their intubation more challenging. We therefore hypothesize that obese trauma patients requiring emergency intubation are at increased risk for unsuccessful intubation and airway-related complications.

Methods: Retrospective review of prospectively collected data from an airway surveillance database at an urban Level I trauma center between 2001 and 2004 was analyzed. The study population included all adult patients admitted to the trauma center, who required urgent airway management. The patients were stratified into four groups according to their body mass index (BMI): lean (BMI <25), overweight (25 <= BMI < 30), obese (30 <= BMI <= 40), and morbid obesity (BMI >40). Demographic parameters and outcome measures including field intubation success, airway complications, early respiratory complications, and mortality were collected. Logistic regression was performed to determine predictors of these outcome measures.

Results: Of the 9,980 patients evaluated during the three-year study period, 1,435 (14%) were emergently intubated and made up the study population. About 92% of ED intubations were performed by the anesthesia team. Of all emergently intubated patients, 46% were lean, 37% were overweight, 15% were obese, and 2% were morbidly obese. There were no significant differences in demographic parameters between the lean, overweight, and obese groups. The morbidly obese patients were however older, composed of more female patients and more likely to have suffered a blunt injury. Logistic regression analysis revealed that BMI was not an independent risk factor for failed intubations in the field or in the ED, postintubation airway complications, or death. Only early respiratory complications demonstrated a statistically significant (p = 0.02), but unlikely clinically relevant (OR = 1.04; 95% CI, 0.99-1.07) association with a higher BMI.

Conclusion: Emergency intubation of obese trauma patients can be safely and successfully performed in a high volume Level I trauma center. Obesity is not a predictor of postintubation airway complications or mortality. Larger studies are needed to validate these finding in the morbidly obese patients.

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categories: Emergency Medicine

CT or MRI?

by Paul Rega, MD — published on August 19th, 2008
Computed Tomography Alone for Cervical Spine Clearance in the Unreliable Patient-Are We There Yet?
Journal of Trauma-Injury Infection & Critical Care. 64(4):898-904, April 2008.
Menaker, Jay MD; Philp, Allan MD; Boswell, Sharon ACNP; Scalea, Thomas M. MD

Abstract:
Background: Injuries to the cervical spine (CS) occur in 2% to 6.6% of blunt trauma patients. Studies have suggested that computed tomography (CT) alone is sufficient for CS clearance in unreliable patients based on follow-up magnetic resonance (MR) imaging not altering management. We hypothesized that an admission cervical spine CT with no acute injury-using new CT technology-is not sufficient for CS clearance in an unreliable patient.

Methods: The trauma registry was used to identify all patients with blunt trauma who had CS imaging with a CT and MR between August 2004 and December 2005. During this time period, a clinical guideline was in place whereby patients who had persistently unreliable examinations had MR despite a normal admission CT. Medical records were reviewed for demographics, Glasgow Coma Scale (GCS) score at time of MR, and injury specific data.

Results: Seven hundred thirty-four patients in total were identified. Two hundred three patients without obvious neurologic deficits but unreliable clinical examination, defined by a GCS score of <=14, had an initial cervical spine CT read by an attending trauma radiologist as having no acute injury. Mean age was 42.3 years (+/-20.4 years) and mean Injury Severity Score was 29.1 (+/-11.8). There were 135 (66.5%) men. Mechanism of injury included motor vehicle or motorcycle collision (48.8%), falls (25.4%), pedestrians struck (10.2%), assault (7.8%), and other (7.8%). One hundred eighty-four (90.6%) patients had a negative MR and collars were subsequently removed. After collar removal, no patient developed new neurologic deficit. Eighteen (8.9%) patients had an abnormal MR, 2 of which required operative repair and 14 required extended cervical collar use. Two patients had collars removed at the discretion of the attending surgeon. One patient had a suboptimal MR and was discharged in a collar with scheduled follow-up.

Conclusion: Newer generation CT continues to miss CS injuries in unreliable patients. MR changed the management in 7.9% of patients having had an admission CT with no acute injury. Thus, we recommend continued use of MR for CS clearance in the unreliable patient and ongoing evaluation as the quality of CT imaging continues to evolve.

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categories: Emergency Medicine

Choppers effective in TBIs

by Paul Rega, MD — published on August 19th, 2008
Air Medical Response to Traumatic Brain Injury: A Computer Learning Algorithm Analysis.

Original Articles

Journal of Trauma-Injury Infection & Critical Care. 64(4):889-897, April 2008.
Davis, Daniel P. MD, FACEP; Peay, Jeremy MD; Good, Benjamin MS; Sise, Michael J. MD; Kennedy, Frank MD; Eastman, A Brent MD; Velky, Thomas MD; Hoyt, David B. MD

Abstract:
Background: The role of air medicine in traumatic brain injury (TBI) has been studied extensively using trauma registries but remains unclear. Learning algorithms, such as artificial neural networks (ANN), support vector machines (SVM), and decision trees, can identify relationships between data set variables but are not empirically useful for hypothesis testing.

Objective: To use ANN, SVM, and decision trees to explore the role of air medicine in TBI.

Methods: Patients with Head Abbreviated Injury Score 3+ were identified from our county trauma registry. Predictive models were generated using ANN, SVM, and decision trees. The three best-performing ANN models were used to calculate differential survival values (actual and predicted outcome) for each patient. In addition, predicted survival values with transport mode artificially input as “air” or “ground” were calculated for each patient to identify those who benefit from air transport. For SVM analysis, [chi]2 was used to compare the ratio of unexpected survivors to unexpected deaths for air- and ground-transported patients. Finally, decision tree analysis was used to explore the indications for various transport modes in optimized survival algorithms.

Results: A total of 11,961 patients were included. All three learning algorithms predicted a survival benefit with air transport across all patients, especially those with higher Head Abbreviated Injury Score or Injury Severity Score values, lower Glasgow Coma Scale scores, or hypotension.

Conclusion: Air medical response in TBI seems to confer a survival advantage, especially in more critically injured patients.

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categories: Emergency Medicine

Bilateral Hip Fractures

by Paul Rega, MD — published on August 19th, 2008
Simultaneous Bilateral Hip Fractures in a Level I Trauma Center.

Original Articles

Journal of Trauma-Injury Infection & Critical Care. 65(1):132-135, July 2008.
Grisoni, Nicolas MD; Foulk, David MD; Sprott, Dominic MBBS, MRCS; Laughlin, Richard T. MD

Abstract:
Background: Hip fractures are a common occurrence among the population today, especially in the elderly. However, the incidence of simultaneous bilateral hip fractures is very rare, and there is a paucity of data in the current literature documenting patients with these hip fractures.

Methods: A retrospective case review was performed on all patients treated for hip fractures during the past ten years at our Level I trauma center.

Results: From 1993 to 2002 there were eight patients who sustained simultaneous bilateral hip fractures. The mean age of the patients was 63 years (range, 34-88 years). The overall survival rate was 63%. In the patients of age group younger than 65, the survival rate was three out of four (75%). In the patients of age group 65 and older, the survival rate was two of four (50%). The length of hospital stay was shorter on average for the younger population, 19 days (range, 17-27 days). The average hospital duration for the older population was 29 days (range, 28-30).

Conclusion: Bilateral hip fractures are usually the result of a high-energy trauma and are associated with other injuries. The morbidity and mortality of this injury are quite high. Patient age, associated injuries, and comorbid conditions should be examined closely because they may influence the patient’s recovery.

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categories: Emergency Medicine

Greenfield filters effective in pelvic trauma patients

by Paul Rega, MD — published on August 19th, 2008

Long-Term Consequences of Pelvic Trauma Patients With Thromboembolic Disease Treated With Inferior Vena Caval Filters.
Journal of Trauma-Injury Infection & Critical Care. 65(1):25-29, July 2008.
Toro, Jose B. MD; Gardner, Michael J. MD; Hierholzer, Christian MD; Sama, Domenico MD; Kosi, Cagri MD; Ertl, William MD; Helfet, David L. MD

Abstract:
Background: The use of inferior vena cava (IVC) filters for prevention of pulmonary embolism (PE) in high-risk trauma patients is well accepted. High rates of recurrent venous thrombosis, however, and postthrombotic syndrome (PTS) have been reported in nonsurgical patients with medical comorbidities. Patients with pelvic trauma and thromboembolic disease have a unique thrombogenic pathophysiology, and the long-term consequences of filter placement in these patients are unknown. We sought to evaluate the outcomes of patients who sustained pelvic trauma, and who developed venous thrombosis and were treated with a vena caval filter.

Methods: A cohort of 102 consecutive patients was treated for a pelvic or acetabular fracture who developed deep vein thrombosis (DVT) preoperatively and had a caval filter placed. Thromboembolic events and complications were evaluated by both retrospective chart review and a prospective questionnaire. Eighty-eight patients (86%) returned the questionnaire at an average follow-up of 4 years.

Results: No patients were readmitted to the hospital for recurrent venous thrombosis or PE. Six patients (7%) described new swelling in the lower extremities, and one (1%) demonstrated evidence of PTS. No deaths occurred related to PE.

Conclusions: The use of IVC filters appears to be safe and effective in preventing PE in patients with pelvic trauma and established venous thrombosis. The risk of recurrent DVT is low and PTS is negligible in these patients. Filter placement use is not associated with the same long-term complications as in patients with thrombosis because of chronic medical comorbidities.

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categories: Emergency Medicine

Methotrexate & Ectopics

by Paul Rega, MD — published on August 19th, 2008

http://www.medscape.com/viewarticle/576935_print

Question
When is it appropriate to use methotrexate for ectopic pregnancy in the emergency department?

Answer from Noelle Rotondo, DO
Associate Professor, Penn State Hershey Medical Center, Hershey, Pennsylvania; Staff Physician, York Hospital, York, Pennsylvania

Methotrexate is a chemotherapeutic agent used as medical therapy for the treatment of ectopic pregnancy. Although it is most commonly administered intramuscularly, obstetricians may inject the medication directly into the ectopic fetus under ultrasound guidance.[1] This discussion will focus on the use of methotrexate in the emergency department (ED), where it is most commonly administered via intramuscular injection.

Methotrexate is a folic acid antagonist that acts by blocking dihydrofolate reductase. In turn, it prevents cell division in rapidly dividing fetal cells. The decision to use methotrexate in the ED should be made in consultation with the patient’s obstetrician, who will be responsible for continued outpatient management.

Indications for methotrexate therapy include[2]:

  • Hemodynamic stability and no evidence of ectopic rupture;
  • Gestational sac ≤ 4 cm if no cardiac activity;
  • Gestational sac ≤ 3.5 cm if cardiac activity is present;
  • Reliable patient, able to follow up for appointments and laboratory studies; and
  • Beta-human chorionic gonadotropin (beta-hCG level) ≤ 5000 mIU/mL.

The failure rate of methotrexate, or the percentage of patients who will require surgical therapy following treatment, increases proportionately as initial beta-hCG levels increase.[3] For patients who have an initial beta-hCG level < 1000 mIU/mL, single-dose methotrexate therapy has a failure rate of just 1.5%. When levels are between 1000 and 5000 mIU/mL, the failure rate is 4%. The failure rate jumps to 14% with initial beta-hCG levels of 5000 to 9999 mIU/mL, and up to 18% with levels between 10,000 and 15,000 mIU/mL.[3]

Contraindications to methotrexate therapy include the following[2]:

  • Evidence of ectopic rupture (clinically or on ultrasound);
  • White blood cell count ≤ 1500/mm3;
  • Creatinine > 1.5 mg/dL;
  • Aspartate aminotransferase (AST) > 2 times upper limits of normal;
  • Platelet count <100,000/mm3; and
  • Patient unreliable or unable to follow up for appointments.

Two commonly used methotrexate protocols are single-dose, which has an 88.1% success rate or multidose, which has a 92.7% success rate.[2,4,5] The single-dose protocol is more commonly used because it is associated with fewer side effects, is less expensive, requires fewer physician visits, and has greater patient compliance.[2,4,5] “Single-dose” therapy is something of a misnomer, however, because approximately 20% of patients will require repeat outpatient injections.[4]

Methotrexate has potentially serious side effects, including bone marrow suppression, liver cirrhosis, renal failure, and pulmonary fibrosis. However, these side effects are generally seen at much higher doses (ie, chemotherapeutic doses) than those used for the treatment of ectopic pregnancy.[4] Regardless, all patients should have a baseline complete blood count, liver function tests, and renal profile checked prior to treatment.

The most common side effects of methotrexate at doses used to treat ectopic pregnancy include excessive flatulence, abdominal pain (that may mimic a ruptured ectopic pregnancy), stomatitis, and sometimes a mild transient elevation of liver enzymes.[1] Patients are instructed to abstain from sexual intercourse (which could increase their risk for rupture), avoid potential gas-producing foods (cabbage, broccoli), and abstain from alcohol. Excessive flatulence is treated with over-the-counter antigas medication. Stomatitis may be treated with “magic mouthwash.” The mouthwash formulation we use at our institution consists of one third viscous lidocaine 2%, one third diphenhydramine liquid, and one third aluminum hydroxide-magnesuim hydroxide. Instruct the patient to “swish and spit” 1 to 2 tablespoons every 4 to 6 hours as needed.

Patients are instructed to call their obstetrician with any increased abdominal pain or return to the ED with any worsening symptoms such as dizziness, lightheadedness, or increased abdominal pain, which may suggest a ruptured ectopic pregnancy. The risk for tubal rupture with methotrexate therapy is about 5%. Patients who return to the ED with abdominal pain must be evaluated for possible ruptured ectopic pregnancy.

In summary, methotrexate is appropriate for use as medical therapy for the treatment of ectopic pregnancy in select patients in the ED and is administered as a single-dose intramuscular injection. Patients are instructed to follow up with their obstetrician for continued monitoring, and sometimes they require subsequent doses of methotrexate. The most important predictor of success (termination not requiring surgery) with methotrexate is an initial beta-hCG level of 5000 mIU/mL or less on presentation. Although some abdominal pain is a common side effect of methotrexate therapy, patients who experience increased abdominal pain, lightheadedness, dizziness, or syncope need to be reevaluated for the possibility of tubal rupture.

 

References

  1. Raughley MJ, Frishman GN. Local treatment of ectopic pregnancy. Semin Reprod Med. 2007;25:99-116. Abstract
  2. Lipscomb GH. Medical therapy for ectopic pregnancy. Semin Reprod Med. 2007;25:93-98. Abstract
  3. Menon S, Colins J, Barnhart KT. Establishing a human chorionic gonadotropin cutoff to guide methotrexate treatment of ectopic pregnancy: a systematic review. Fertil Steril. 2007;87:481-484. Abstract
  4. Lipscomb GH, Givens VM, Meyer NL. Comparison of multidose and single-dose methotrexate protocols for the treatment of ectopic pregnancy. Am J Obstet Gynecol. 2005;192:1844-1848. Abstract
  5. Farquhar CM. Ectopic pregnancy. Lancet. 2005;366:583-591. Abstract
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categories: Emergency Medicine

More info on Spinal Headaches

by Paul Rega, MD — published on August 19th, 2008

http://www.medscape.com/viewarticle/578254_print

1 Sprotte and Whitacre cause fewer spinal headaches.

1 

Table 1. Risk Factors for Development of PDPH

 

 

1 

Table 2. Things the Emergency Physician Can Do To Reduce PDPH

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categories: Emergency Medicine

The Spinal Headache

by Paul Rega, MD — published on August 19th, 2008

MedScape (http://www.medscape.com/viewarticle/578254_print)

Lumbar Puncture and Post-Dural Puncture Headaches: Implications for the Emergency Physician
Robert L. Frank, MD, FAAEM

 

J Emerg Med.  2008;35(2):149-157.  ©2008 Elsevier Science, Inc.

Posted 08/12/2008

Abstract and Introduction

Abstract

Lumbar puncture is a diagnostic procedure commonly performed by emergency physicians. Post-dural puncture headaches occur frequently after this procedure and can be associated with significant morbidity and, occasionally, even death. There is also a lot of variation in how post-dural puncture headaches are treated once they occur. This article seeks to examine the science behind post-dural puncture headaches, their prevention and treatment.

Introduction

Post-dural puncture headache (PDPH) is the most common complication of procedures in which the dura is penetrated, such as diagnostic lumbar punctures, spinal anesthetics, myelograms, and inadvertent dural punctures during epidural injections.[1] PDPH was first described in 1898 by August Bier, who experienced this condition first hand after experimentation with spinal anesthesia with co-pioneer August Hildebrandt.[2] Patients with PDPHs often present to the Emergency Department to seek care for this condition. Additionally, emergency physicians frequently perform diagnostic lumbar punctures, thus putting these patients at risk for PDPH. Because emergency physicians are often faced with treating PDPHs, it is imperative that they are able to accurately diagnose them and are familiar with the available therapies and their effectiveness and risks. Additionally, are there techniques that emergency physicians should utilize in the performance of lumbar punctures to minimize the incidence of PDPHs? This article seeks to examine the science behind these issues.

Anatomy and Physiology

The spinal cord is bathed in cerebrospinal fluid (CSF). The CSF is contained within the dura mater, which extends from the foramen magnum to the second sacral spinal segment. The dura mater is a tubular structure made of dense collagen and elastic fibers. It was originally thought that the fibers were oriented in a direction parallel to the spine, but more recent studies using electron microscopy have shown no particular or consistent pattern of the dural fibers.[3,4] The thickness of the posterior dura is also variable and unpredictable, which may have implications in the occurrence of PDPHs.[3] The normal volume of CSF in the adult is 150 mL, and several times this amount is secreted and reabsorbed by the choroid plexus daily.[5] The arachnoid mater is a thin layer of tissue that is loosely adherent to the under surface of the dura.

Pathophysiology

The headache that ensues after dural puncture is theorized to be primarily due to loss of CSF from a defect made in the dura with resultant intracranial hypotension.[6] A large defect allows for greater loss of CSF and increases the likelihood of intracranial hypotension and PDPH.[7] When the patient then assumes an upright position there is downward traction on pain-sensitive intracranial veins, meninges, and cranial nerves caused by gravity and loss of buoyancy from the reduced CSF pressure.[8,9,10] This “sagging” of intracranial structures has been demonstrated on magnetic resonance imaging.[11] CSF leak after dural puncture has been well documented.[12] Manometric studies have demonstrated that adult subarachnoid pressure is reduced from the normal 5-15 cm H2O to < 4 cm H2O, and the rate of CSF leak is generally greater than CSF production.[12] Support for this theory of PDPH also lies in the fact that intrathecal or epidural injections of saline restore the CSF volume, increase epidural and subarachnoid pressure, and alleviate the headache.[13,14] Other proposed mechanisms for the pain of PDPH include a resultant dilatation of the cerebral blood vessels as a compensatory mechanism to restore intracranial volume, which may further exacerbate the symptoms.[6] Clark also found that patients with low CSF levels of the neurotransmitter substance P, which is released with dural puncture, were three times more likely to have PDPHs than those with higher levels.[15] Hypersensitivity to substance P with upregulation of receptors is thought to be a causative factor in post-dural puncture as well as other types of headache.

Incidence

PDPHs occur with a wide range of reported frequency, from <1% in some studies to as much as 70% in others.[16,17] This wide range is due to the fact that certain patient populations and dural puncture procedures carry quite variable degrees of risk for PDPH. Patients who receive dural punctures with large-bore needles (diagnostic myelography and inadvertent dural puncture during labor epidural anesthesia) are very likely to sustain PDPHs. Patients who receive spinal anesthesia with small (24-30-gauge) non-cutting needles generally have significantly reduced risk of PDPH, with rates as low as 2% or less.[7] PDPH after diagnostic lumbar puncture (excluding myelography, pneumoencephalography, and cisternal puncture) has an incidence of 6-40%.[9,18,19,20,21] This number is reduced to about 5% when special measures are taken to reduce PDPH.[22,23]

Symptoms

Although PDPHs can occur from immediately to months after dural puncture, 90% occur within the first 72 h and most within 48 h.[24,25] Headaches that occur beyond this time frame should raise suspicion for other causes. PDPH is typically frontal or occipital, “burning,” and radiates into the neck and shoulders.[5] Pain, though, may be in any location in the head or neck.[26,27] Isolated back pain may infrequently be the presenting complaint.[28] The most important diagnostic feature is that the headache is minimal or absent in the supine position and is exacerbated with upright posture.[5] If this component is not present, diagnosis of PDPH should be reconsidered. PDPH is often associated with nausea and vomiting, photophobia, diplopia, low back pain, neck stiffness, dizziness, tinnitus, hearing changes, and cranial nerve palsies.[27,28,29,30] PDPHs can be quite variable in their severity and duration. Seventy-two percent of PDPHs will resolve spontaneously in 7 days.[31] Case reports have documented a PDPH lasting as long as 8 years.[32] The headache may be mild and resolve spontaneously in a few days, or severe, lasting a week or longer and causing significant disability. A study by Tohmo et al. found that 39% of patients with PDPH had 1 week of impaired ability to perform activities of daily living.[33] Additionally, PDPHs that persist untreated can predispose to subdural hematoma, herniation, and death.[34,35,36]

Diagnosis

Diagnosis of PDPH is usually a clinical diagnosis, generally aided by the history that there has been some recent procedure with actual or potential risk of dural puncture. This may include diagnostic lumbar puncture, myelogram, spinal anesthetic, epidural anesthetic or steroid injection, and spine surgery. A characteristic positional headache is also essential. Various imaging techniques to aid diagnosis have been described but are rarely needed except to rule out other causes of headache.[37,38] In the postpartum period, other causes of headache such as preeclampsia, posterior leukoencephalopathy, caffeine withdrawal, migraine, and cocaine abuse should be considered. A procedure described by Gutsche also may be helpful in patients in whom the diagnosis of PDPH is uncertain.[39] Firm continuous abdominal pressure is applied with the examiner’s hand while the headache is present. A PDPH will usually be significantly relieved within 30 s and return when pressure is released. This is thought to be due to an increase in pressure relieving CSF hypotension.

Risk Factors for PDPH

Demographic and Other Risk Factors

There are certain demographic factors that seem to be associated with risk of PDPH for reasons that are not well understood. Patient age is a risk factor, with ages between 18 and 40 years the highest risk range.[26,32,40,41,42] The risk of PDPH at age 25 years is 3-4 times that at age 65 years.[31,42,43] Children younger than 13 years rarely get PDPH.[44,45] This is thought to be due to lower CSF pressure in children.[46,47] PDPHs do occur with increasing frequency in adolescents and are similar to those seen in adults.[48,49] There is also significantly decreased frequency after age 60 years, which also may be related to reduced CSF pressure.[50] Female sex, regardless of age, is also a risk factor for PDPH for unknown reasons. Women have approximately twice the likelihood compared to men.[18,31,51] Race does not seem to be a factor in development of PDPH.[25] A history of chronic or recurrent headache has been found in nearly 60% of those with PDPH.[15] Previous history of PDPH is also a risk factor for development of future headaches.[43] Although there is a high incidence of pregnancy-related PDPHs, a meta-analysis by Morewood did not show that pregnancy in and of itself was likely to be the cause.[9] The increased frequency may be more likely related to patient age and sex. Inadvertent dural puncture during the performance of labor epidural anesthesia significantly increases the risk of PDPH, but even in pregnant women who receive only spinal anesthesia, the risk of PDPH is considerably elevated. Volume of CSF removed and its role in causing PDPH is unclear. Removal of 15-20 mL of CSF reliably caused headaches in one study.[26] Volume of CSF removed did not seem to be a factor in a study by Kuntz et al..[18] The small volume usually removed during diagnostic lumbar punctures performed by emergency physicians is not likely to be a significant factor. Experience of the practitioner performing the dural puncture does not seem to be a factor in development of PDPH, nor does multiple attempts at lumbar puncture.[52] Low body mass index is another a risk factor for PDPH.[18] Thus, young, thin women seem to be at highest risk for PDPH. These results are summarized in Table 1 .

Spinal Needles and Their Relationship to PDPH

Size of Spinal Needle

There are several characteristics related to the spinal needle used that are critical determinants in development of PDPH. Although these issues have long been part of anesthesia practice, they are rarely considered by other specialists who perform dural puncture procedures.[53,54,55] Thoughtful consideration of these issues is one area in which emergency physicians can have a significant impact on reducing the occurrence of PDPHs. The first issue relates to size of the needle. Larger needles leave larger holes, allow for greater CSF leak and, thus, cause more PDPHs.[7,43,50,53,56,57] The incidence of PDPH with the standard 20- or 22-gauge Quincke cutting beveled needle commonly used by non-anesthetists for diagnostic lumbar puncture is as high as 40%.[9,18,19,20,21] This could be reduced to as low as 5% using a similar 24-27-gauge needle.[58] It has been a long-held belief that the small needles used for performance of spinal anesthetics allow for too-slow fluid collection and unacceptable difficulty for use in the performance of diagnostic lumbar punctures.[7] Carson and Serpell found that use of needles smaller than 22-gauge required >6 min to collect 2 mL of CSF and measurement of opening pressure was similarly slow and potentially inaccurate.[7] Thus, it is felt by some that needles smaller than 22-gauge are inadequate for diagnostic lumbar punctures.[59] Strachan et al., however, showed that 2 mL of CSF could be obtained by gentle aspiration through a 24-gauge needle in <1 min.[60] In addition to using a smaller-gauge needle, using a needle with an atraumatic tip can further reduce the incidence of PDPH, as will be discussed below.

Needle Shape

An additional factor important in reducing PDPH is the shape of the tip of the spinal needle. Green, in 1926, showed that blunt-tipped spinal needles that separate dural fibers and allow recoil with minimal tearing significantly reduce CSF leak and PDPH.[61] Holst et al. showed with electron microscopy that atraumatic needles leave smaller holes in the dura that tend not to remain open and have three times less CSF leakage than Quincke (BD, Franklin Lakes, NJ) needles.[62] In recent years, several atraumatic (also known as pencil point or non-cutting) spinal needles have been introduced, with the Sprotte (B. Braun Medical Inc., Bethlehem, PA) and Whitacre (BD, Franklin Lakes, NJ) brands being most commonly used (Figure 1). The anesthesia literature has shown conclusively that atraumatic needles significantly reduce incidence of PDPH compared to cutting Quincke-type needles typically used by non-anesthesia practitioners.[53] Although less studied in diagnostic lumbar puncture, there is evidence to support the use of atraumatic needles for PDPH reduction. Thomas et al. showed that PDPH incidence could be reduced from 54% to 29% if a 20-gauge atraumatic needle was used rather than a Quincke cutting beveled needle.[63] The incidence could be further reduced to 4% when 22-gauge atraumatic spinal needles are used.[23] Strupp et al. found that patients who received a diagnostic lumbar puncture with a 22-gauge atraumatic needle had a PDPH rate of 12.2% vs. 24.4% in those who received lumbar puncture with a 22-gauge Quincke needle.[19] Other investigators have shown similar reductions in PDPH with the use of 22-gauge atraumatic needles.[54,64,65] Other studies have not shown a reduction in PDPH when atraumatic needles were compared to similar-gauge cutting beveled needles. Lenaerts et al. found no benefit when the 20-gauge atraumatic Sprotte needle was compared to the 20-gauge cutting Yale needle (BD Madrid, Spain).[66] These findings are likely related to the fact that even though an atraumatic needle was used, it was a large-bore needle that would cause a sizeable dural rent despite its non-cutting tip. Other investigators also have found no reduction in PDPH after diagnostic lumbar puncture when atraumatic 22-gauge needles were compared with cutting Quincke needles.[67,68] Disadvantages of the atraumatic needles includes increased cost, different “feel” and lack of “pop” that is often felt upon piercing the dura, occasional failure to obtain CSF, and difficulty penetrating the skin due to the dull tip. This last issue can be overcome by insertion of the atraumatic spinal needle through a traditional cutting 18-gauge needle acting as an introducer placed beyond the epidermis. Taking into consideration the desirable characteristics of a spinal needle for use in diagnostic lumbar puncture and the goal of reducing the risk of PDPH, a 24-gauge atraumatic needle may be the needle of choice, especially for those at high risk for PDPH. Atraumatic needles are slightly more expensive than similar Quincke needles (approximately $12 versus $4, respectively), although this cost could be easily offset by the reduced numbers of spinal headaches.[20]

Bevel Orientation

Another factor that significantly reduces likelihood of PDPH when using a cutting beveled Quincke needle is the orientation of the needle tip to the dura. Although the dural fibers in general have no consistent orientation, branching elastic fibers do tend to lie in an orientation that minimizes the size of the opening when the cutting bevel of the needle is inserted parallel to the long axis of the spine.[3,4] This causes fewer fibers to be cut than if the bevel were inserted in a perpendicular orientation. Thus, a smaller hole in the dura is created, less CSF leakage occurs, and there is reduced likelihood of PDPH.[43,52,55,69,70,71] Therefore, insertion of the needle with the cutting bevel parallel to the long axis of the spine is indicated. Tearing of the dura may also occur upon removal of the needle if it is rotated to a perpendicular orientation after insertion.[72] Bevel orientation is not an issue with atraumatic needles, as they tend to separate dura fibers rather than cutting them, allowing them to return to their original position with decreased CSF leakage.[61]

Stylet Replacement

Replacement of the spinal needle stylet before removal of the needle also has been shown to reduce the incidence of PDPH. Strupp et al. found that stylet reinsertion reduced PDPH from 16% to 5% with 21-gauge Sprotte atraumatic needles.[19] It was postulated that a strand of arachnoid mater may be pulled by the open needle on its removal and enter the dural rent, maintaining an opening that allows greater CSF leakage.[19] A similar study has not been performed using cutting Quincke needles. A similar effect may occur if the spinal needle strikes bone upon insertion. This has been reported to cause a burr to develop at the needle tip that will drag the arachnoid mater out as it is withdrawn, thus creating a CSF leak.[73] This concept has not been formally studied.

Bed Rest

Use of bed rest to prevent PDPH was first advocated by Bier in 1899.[20] It is still advocated by many that a patient must have some period of bed rest after a lumbar puncture to prevent PDPH. A meta-analysis by Thoennisen et al. and a Cochrane review by Sudlow and Warlow evaluated all studies on this topic and found no difference in incidence of PDPH for those with immediate mobilization vs. bed rest for up to 24 h.[29,74] Thus, bed rest after lumbar puncture has no role in PDPH prevention.

Hydration

It is advocated by some that increased hydration after dural puncture will minimize PDPH occurrence, possibly by increasing the rate of production of CSF to replace the fluid lost from leakage. This was not found to be beneficial in the only study that has examined this issue.[75] Thus, it would seem that intake of additional fluids after a lumbar puncture does not assist in PDPH prevention.[76]

Patient Positioning During Lumbar Puncture

The position that the patient is placed in during LP has been postulated to play a role in the development of PDPH.[77] A controlled study did not show the position used during performance of LP to have a relationship to development of PDPH.[78] Strategies the emergency physician can employ to reduce the risk of PDPH are summarized in Table 2 .

Treatment of PDPH

Treatment options for dural puncture headache depend on many factors such as severity of headache, degree of interference with activities of daily living, associated symptoms, response to conservative care, and presence of potential contraindications to more definitive therapies. Multiple treatment regimens have been advocated with varying degrees of success and risk, including medications and epidural blood patches ( Table 3 ).

Methylxanthine Derivatives

Methylxanthine derivatives such as caffeine and aminophylline have been recommended for the treatment of PDPH. It has been postulated that at least part of the pain from PDPH is due to cerebral vasodilatation as a compensatory attempt to restore intracranial volume.[6] It is thought that methylxanthine medications cause vasoconstriction of these vessels, thus decreasing pain. It has also been theorized that these drugs antagonize purine receptors and relieve headache by this mechanism.[25] Caffeine is usually given as 500-mg caffeine sodium benzoate in 1 L of intravenous fluid over 1 h, although some have given it as a rapid intravenous bolus.[79,80] A second dose usually can be repeated in 1-2 h if needed. If aminophylline is used, it is given 5-6 mg/kg over 20 min or given orally as theophylline 300 mg every 6-8 h.[25] Side effects include central nervous system stimulation, seizures, gastric irritation, and provocation of cardiac dysrhythmias.[80] Methylxanthine medications have been reported to be effective in alleviating PDPH in up to 90% of patients.[79,80,81,82,83,84,85,86] Unfortunately, the data used to support the efficacy of caffeine are limited to one oft-cited small, methodologically flawed study and several case reports.[73,76,77,80,82,84,86,87,88,89] The effects of caffeine seem to be temporary at best, with headache recurrence rates of up to 60%.[9,83,86,89] It has no effect on CSF leakage nor does it restore normal CSF dynamics, which are thought to be the primary causes of PDPH.[5] Camann et al. found oral caffeine to provide significantly better pain relief than placebo for PDPH initially, but there was no significant difference in pain scores at 24 h or in the number of epidural blood patches performed between the two groups.[89] A recent North American hospital survey reports that most practitioners have abandoned the use of caffeine for treatment of PDPH due to its perceived ineffectiveness. Additionally, although it is sometimes recommended that patients consume caffeine after a lumbar puncture to prevent PDPH, it seems that this strategy, too, is ineffective.[90] Further quality investigation is needed to determine the effectiveness of caffeine and theophylline in the prevention and treatment of PDPH.

Sumatriptan

Sumatriptan is a serotonin agonist occasionally used in the treatment of migraines. It has been reported successful for the treatment of PDPH.[43,91,92] Others have found it to be ineffective.[93] A controlled trial found no evidence of benefit when using sumatriptan in the treatment of PDPH.[94]

Epidural Blood Patch

Despite a recent Cochrane review that was unable to draw unequivocal conclusions about its efficacy, the epidural blood patch (EBP) is generally considered the definitive treatment for PDPH, especially for those that are severe or debilitating.[5,16,29,43,44,81,95,96,97,98,99] It was first described in 1960 by Gormley after it was noted that “bloody taps” were associated with decreased incidence of PDPH.[100] EBP is performed by injecting 15-30 mL of the patient’s blood into the epidural space through a Tuohy epidural needle.[16] This is ideally done at the site of the previous dural puncture. The injected blood spreads in both a cranial and caudal direction. The thecal sac is compressed and displaced and is thought to elevate and thus restore the subarachnoid pressure.[5] It is also thought that the blood clot that forms seals off the rent in the dura and prevents further leakage of CSF. Success rates have generally been reported in 72-98% of patients, although less favorable results have been noted.[1,16,39,81,97,98,101,102,103,104,105] Usually, there is immediate relief of the headache. EBP is most effective when performed at least 24 h after the initial puncture.[25] Complications are rare but include radicular pain from nerve root irritation or displacement, cranial nerve palsies, meningeal irritation, elevated intracranial pressure, paraparesis, cauda equina syndrome, infection, and subdural hematoma.[5,106,107,108] Complications are usually either rare or self-limited. Contraindications to EBP include patient refusal, fever or suspected bacteremia and anticoagulation.[5,108] EBP has been successfully used in adolescents.[48] Patients who get no or incomplete relief after a first EBP have equivalent or higher rates of success on a second attempt.[25,102] Failure of EBP is seen most often in patients with dural puncture from large bore needles, such as with inadvertent dural puncture with 16-gauge Tuohy needles during performance of labor epidural anesthesia.[1,102]

Prophylactic Epidural Blood Patch

Some practitioners advocate use of a “prophylactic” EBP to prevent PDPH, especially in those at high risk (partiuent with inadvertent dural puncture with a large bore epidural needle). The datasupporting this practice are contradictory. Several studies have shown benefit, others have not.[109,110,111,112] A recent Cochrane review found there were insufficient quality data to reach a definitive conclusion on the effectiveness of this practice.[29] This practice is not likely to have much impact on the prevention of PDPH from diagnostic lumbar punctures performed by emergency physicians.

Conclusions

Dural puncture procedures are commonly performed by various medical practitioners, including emergency physicians, for many reasons. PDPH is a relatively common complication. The degree of pain and disability caused by PDPHs is considerable. Appropriate use of smaller-gauge, atraumatic needles is likely the single most important factor in reducing PDPH. Hydration and bed rest do little to prevent PDPH. Treatment of mild, non-debilitating headaches usually can be accomplished with limited activity, analgesics, and methylxanthine therapy until they resolve spontaneously. For more severe headaches, methylxanthine derivatives may be tried with EBP as a first-line alternative or to be used if methylxanthines fail. It is helpful to use 24-gauge Sprotte spinal needles in all patients at risk for PDPH. For patients who have moderate to severe pain, cannot or do not want to remain on bed rest, and those in whom narcotic pain medication is not a practical treatment option, EBP is an appropriate first-line therapy. In general, EBP is safe, well tolerated and effective. Though the technique for epidural blood patch is not significantly more difficult than lumbar puncture, it is a procedure most commonly performed by anesthesiologists.

References

  1. Vercauteren MP, Hoffman VH, Mertens E, Sermeus L, Adriaensen HA. Seven-year review of requests for epidural blood patches for headache after dural puncture: referral patterns and the effectiveness of blood patches. Eur J Anaesthesiol 1999;16: 298–303.
  2. Calverley RK. Anesthesia as a specialty: past, present, and future. In: Barash PG, Cullen BF, Stoelting RK, eds. Clinical anesthesia. Philadelphia, PA: Lippincott; 1989:35– 42.
  3. Reina MA, de Leon-Casasola OA, Lopez A, De Andres J, Martin S, Mora M. An in vitro study of dural lesions produced by 25-gauge Quincke and Whitacre needles evaluated by scanning electron microscopy. Reg Anesth Pain Med 2000;25:393– 402.
  4. Fink BR, Walker S. Orientation of fibers in human dorsal lumbar dura mater in relation to lumbar puncture. Anesth Analg 1989; 69:768 –72.
  5. Turnbull DK, Shepherd DB. Post-dural puncture headache: pathogenesis, prevention and treatment. Br J Anaesth 2003;91: 718–29.
  6. Grant R, Condon B, Hart I, et al. Changes in intracranial CSF volume after lumbar puncture and their relationship to post-LP headache. J Neurol Neurosurg Psychiatry 1991;54:440 –2.
  7. Carson D, Serpell M. Choosing the best needle for diagnostic lumbar puncture. Neurology 1996;47:33–7.
  8. Peterman SB. Postmyelography headache: a review. Radiology 1996;200:765–70.
  9. Morewood GH. A rational approach to the cause, prevention and treatment of postdural puncture headache. Can Med Assoc J 1993;149:1087–93.
  10. Hilton-Jones D. Post lumbar puncture headache. Springfield IL: Charles C. Thomas; 1964.
  11. Hannerz J, Ericson K, Bro Skejø HP. MR imaging with gadolinium in patients with and without post-lumbar puncture headache. Acta Radiol 1999;40:135– 41.
  12. Rando TA, Fishman RA. Spontaneous intracranial hypotension: report of two cases and review of the literature. Neurology 1992;42:481–7.
  13. Charsley MM, Abram SE. The injection of normal saline reduces the severity of postdural puncture headache. Reg Anesth Pain Med 2001;26:301–5.
  14. Usubiaga JE, Usubiaga LE, Brea LM, et al. Effect of saline injection on epidural and subarachnoid space pressures and relation to postspinal anesthesia headache. Anesth Analg 1967;46: 293–6.
  15. Clark JW. Substance P concentration and history of headache in relation to postlumbar puncture headache: towards prevention. J Neurol Neurosurg Psychiatry 1996;60:681–3.
  16. Crawford J. Experiences with epidural blood-patch. Anaesthesia 1980;35:513–5.
  17. Fishman RA. CSF in diseases of the nervous system. Philadelphia, PA: WB Saunders; 1992.
  18. Kuntz KM, Kokmen E, Stevens JC, et al. Post-lumbar puncture headaches: experience in 501 consecutive procedures. Neurology 1992;42:1884 –7.
  19. Strupp M, Schueler O, Straube A, et al. “Atraumatic’ Sprotte needle reduces the incidence of post-lumbar puncture headaches. Neurology 2001;57:2310 –12.
  20. Evans RW, Armon C, Frohman E, et al. Assessment: prevention of post-lumbar puncture headaches: report of the therapeutics and technology assessment subcommittee of the American Academy of Neurology. Neurology 2000;55:909 –14.
  21. Seupaul RA, Somerville GG, Viscusi C, et al. Prevalence of postdural puncture headache after ED performed lumbar puncture. Am J Emerg Med 2005;23:913–5.
  22. Candido KD, Stevens RA. Post-dural puncture headache: pathophysiology, prevention and treatment. Best Pract Res Clin Anes 2003;17:45– 69.
  23. Braune HJ, Huffmann G. A prospective double-blind clinical trial, comparing the sharp Quincke needle (22G) with an “atraumatic’ needle (22G) in the induction of post-lumbar puncture headache. Acta Neurol Scand 1992;86:50–4.
  24. Weir EC. The sharp end of the dural puncture. Br Med J 2000; 320:127– 8.
  25. Leibold RA, Yealy DM, Coppola M, et al. Post-dural-puncture headache: characteristics, management and prevention. Ann Emerg Med 1993;22:1863–70.
  26. Davignon KR, Dennehy KC. Update on postdural puncture headache. Int Anesthesiol Clin 2002;40:89 –102.
  27. Cooper G. Epidural blood patch. Eur J Anaesthesiol 1999;16: 211–5.
  28. Dunbar SA, Katz NP. Post-dural puncture thoracic pain without headache: relief with epidural blood patch. Can J Anaesth 1995; 42:221–3.
  29. Sudlow C, Warlow C. Epidural blood patching for preventing and treating post-lumbar puncture headache. Cochrane Database Syst Rev 2002;2:CD001791.
  30. Weeks SK. Postpartum headache. In: Chestnut DH, ed. Obstetric anesthesia: principles and practice, 2nd edn. St. Louis, MO: Mosby; 1999:621–38.
  31. Vandam LD, Dripps RD. Long-term follow up of patients who received 10,098 spinal anesthetics. JAMA 1956;161:586 –91.
  32. MacArthur C, Lewis M, Knox EG. Accidental dural puncture in obstetric patients and long term symptoms. Br Med J 1992;304: 1279–82.
  33. Tohmo H, Vuorienen E, Muuronen A. Prolonged impairment in activities of daily living due to postdural puncture headache after diagnostic lumbar puncture. Anaesthesia 1998;53:299 –302.
  34. Edelman JD, Wingard DW. Subdural haemoatomas after lumbar dural puncture. Anesthesiology 1980;52:166 –7.
  35. Lance JW, Branch GB. Persistent headache after lumbar puncture. Lancet 1994;343:414.
  36. Eerola M, Kaukinen L, Kaukinen S. Fatal brain lesion following spinal anesthesia. Acta Anesthesiol Scand 1981;25:115– 6.
  37. Mokri B, Parisi JE, Scheithauer BW, et al. Meningeal biopsy in intracranial hypotension: meningeal enhancement on MRI. Neurology 1995;45:1801–7.
  38. Denny N, Masters R, Pearson D, et al. Postdural puncture headache after continuous spinal anesthesia. Anesth Analg 1987;66:791–4.
  39. Gutsche BB. Lumbar epidural analgesia in obstetrics: taps and patches. In: Reynolds F, ed. Epidural and spinal blockade in obstetrics. Oxford, UK: Bailliere Tindall; 1984:95–106.
  40. Vilming ST, Schrader H, Monstad I. The significance of age, sex and cerebrospinal fluid pressure in post-lumbar puncture headache. Cephalgia 1989;9:99 –106.
  41. Solomon GD, Clark JW, deSenanayake P, et al. Hypersensitivity to substance P in the etiology of postlumbar puncture headache. Headache 1995;35:25– 8.
  42. Flaatten H, Rodt S, Rosland J, et al. Postoperative headache in young patients after spinal anesthesia. Anaesthesia 1987;42:202–5.
  43. Lybecker H, Møller JT, May O, Nielsen HK. Incidence and prediction of postdural puncture headache. A prospective study of 1021 spinal anesthesias. Anesth Analg 1990;70:389 –94.
  44. Bolder PM. Postlumbar puncture headache in pediatric oncology patients. Anesthesiology 1986;65:696–8.
  45. Wee LH, Lam F, Cranston AJ. The incidence of post dural puncture headache in children. Anaesthesia 1996;51:1164–6.
  46. Purtock RV, Buhl JL, Abram SE. Epidural blood patch in a nine-year old boy. Reg Anesth 1984;9:154 –5.
  47. Tobias JD. Postdural puncture headache in children— etiology and treatment. Clin Pediatr 1990;33:110 –3.
  48. Ylonen P, Kokki H. Epidural blood patch for management of postdural puncture headache in adolescents. Acta Anaesthesiol Scand 2002;46:794–8.
  49. Aldrete JA. Persistent post-dural-puncture headache treated with epidural infusion of dextran. Headache 1994;34:265–7.
  50. Tourtellotte WW, Henderson WG, Tucker RP, et al. A randomized, double-blind clinical trial comparing the 22 versus 26 gauge needle in production of the post-lumbar puncture syndrome in normal individuals. Headache 1972;12:73– 8.
  51. Kovanen J, Sulkava R. Duration of postdural headache after lumbar puncture; effect of needle size. Headache 1986;26: 224–6.
  52. Flaatten H, Krakenes J, Vedeler C. Post-dural puncture related complications after diagnostic lumbar puncture, myelography and spinal anesthesia. Acta Neurol Scand 1998;98:445–51.
  53. Halpern S, Preston R. Postdural puncture headache and spinal needle design. Anesthesiology 1994;81:1376–83.
  54. Birnbach DJ, Kuroda MM, Sternman D, et al. Use of atraumatic spinal needles among neurologists in the United States. Headache 2001;41:385–90.
  55. Birnbach DJ, Khin N, Sternman D, et al. Differences in the practice of lumbar puncture between anesthesiologists and neurologists. Anesthesiology 1997;87:A988 (Abstract).
  56. Ready LB, Cuplin S, Haschke RH, et al. Spinal needle determinants of rate of transdural fluid leak. Anesth Analg 1989; 69:457– 60.
  57. Dittmann M, Schafer HG, Ulrich J, et al. Anatomic re-evaluation of lumbar dura mater with regard to postspinal headache. Effect of dural puncture. Anaesthesia 1988;43:635–7.
  58. Ball CG, D´Alessandro FT, Rosenthal J, et al. Case history number 86: an unusual complication of lumbar puncture: a CSF cutaneous fistula. Anesth Analg 1975;54:691–2.
  59. Broadley SA, Fuller GN. Lumbar puncture needn´t be a headache: use blunt needles and no bed rest. Br Med J 1997;315: 1324–5.
  60. Strachan A, Train J. Aspirating cerebrospinal fluid speeds up procedure. Br Med J 1998;316:1018 –9.
  61. Green HM. Lumbar puncture and the prevention of post puncture headache. JAMA 1926;86:391.
  62. Holst D, Mollmann M, Ebel C, et al. In vitro investigation of cerebrospinal fluid leakage after dural puncture with various spinal needles. Anesth Analg 1998;87:1331–5.
  63. Thomas SR, Jamieson DRS, Muir KW. Randomized controlled trial of atraumatic versus standard needles for diagnostic lumbar puncture. Br Med J 2000;321:986 –90.
  64. Muller B, Adelt K, Reichmann H, et al. Atraumatic needle reduces the incidence of post-lumbar puncture syndrome. J Neurol 1994;241:376–80.
  65. Pedersen ON. Use of a 22-gauge Whitacre needle to reduce the incidence of side effects after lumbar myelography: a prospective randomised study comparing Whitacre and Quincke spinal needles. Eur Radiol 1996;6:184 –7.
  66. Lenaerts M, Pepin J-L, Tombu S, et al. No significant effect of an “atraumatic’ needle on incidence of post-lumbar puncture headache or traumatic tap. Cephalgia 1993;13:296 –7.
  67. Luostarinen L, Heinonen T, Luostarinen M, et al. Diagnostic lumbar puncture. Comparative study between 22-gauge pencil point and sharp bevel needle. J Headache Pain 2005;6:400–4.
  68. Aamodt A, Vedeler C. Complications after LP related to needle type: pencil-point versus Quincke. Acta Neurol Scand 2001;103: 396–8.
  69. Mihic DN. Postspinal headache and relationship of needle bevel to longitudinal dural fibers. Reg Anesth 1985;10:76–81.
  70. Norris MC, Leighton BL, DeSimone CA. Needle bevel direction and headache after inadvertent dural puncture. Anesthesiology 1989;70:729 –31.
  71. Cruickshank RH, Hopkinson JM. Fluid flow through dural puncture sites: an in vitro comparison of needle point types. Anaesthesia 1989;44:415– 8.
  72. Corbey MP, Bach AB, Lech K, et al. Grading of severity of postdural puncture headache after 27-gauge Quincke and Whitacre needles. Acta Anesthesiol Scand 1997;41:779–84.
  73. Crosby E. Postdural puncture headache. Can Med Assoc J 1994; 150:821–3.
  74. Thoennissen J, Herkner H, Lang W, et al. Does bed rest after cervical or lumbar puncture prevent headache? A systematic review and meta-analysis. Can Med Assoc J 2001;165:1311– 6.
  75. Dieterich M, Brandt T. Incidence of post-lumbar puncture headaches is independent of daily fluid intake. Eur Arch Psychiatry Neurol Sci 1988;237:194–6.
  76. Lin W, Geiderman J. Medical myth: fluids, bed rest, and caffeine are effective in preventing and treating patients with post-lumbar puncture headache. West J Med 2002;176:69 –70.
  77. Brocker RJ. Technique to avoid spinal-tap headache. JAMA 1958;168:261–3.
  78. Vilming ST, Schrader H, Monstad I. Post-lumbar puncture headache: the significance of body posture. A controlled study of 300 patients. Cephalgia 1988;8:75– 8.
  79. Jarvis AP, Greenawalt JW, Fagraeus L. Intravenous caffeine for postdural puncture headache. Anesth Analg 1986;65:316 –7.
  80. Ford CD, Ford DC, Koenigsberg MD. A simple treatment of post-lumbar-puncture headache. J Emerg Med 1989;7:29 –31.
  81. Neal JM. Management of post-dural-puncture headache. Anesthesiol Clin North Am 1992;10:163–78.
  82. Sechzer PH, Abel L. Post-spinal anesthesia headache and treatment with caffeine. Evaluation with demand method. Part I. Curr Ther Res 1976;24:307–12.
  83. Sechzer PH. Post-spinal anesthesia headache treated with caffeine. Part II: intracranial vascular distension. Curr Ther Res 1979;26:440–8.
  84. Harrington TM. An alternative treatment for spinal headache. J Fam Pract 1982;15:172–7.
  85. Hess JH. Postdural puncture headache: a literature review. AANA J 1991;59:549 –55.
  86. Abboud TK, Zhu J, Reyes A, et al. Efficacy of intravenous caffeine for post dural puncture headache. Anesthesiology 1990; 73:A936 (Abstract).
  87. Choi, A, Laurito CE, Cunningham FE. Pharmacologic management of postdural puncture headache. Ann Pharmacother 1996; 30:831–9.
  88. Baumgarten RK. Should caffeine become the first line treatment for postdural puncture headache? Anesth Analg 1987;66:913– 4.
  89. Camann WR, Murray RS, Mushlin PS, et al. Effects of oral caffeine on postdural puncture headache: a double-blind, placebocontrolled trial. Anesth Analg 1990;70:181– 4.
  90. Esmaoglu A, Akpinar H, Ugur F. Oral multidose caffeineparacetamol combination is not effective for the prophylaxis of postdural puncture headache. J Clin Anesth 2005;17:58 – 61.
  91. Carp H, Singh PJ, Vadhera R, et al. Effects of the serotoninreceptor agonist sumatriptan on postdural puncture headache: report of six cases. Anesth Analg 1994;79:180 –2.
  92. Stallard N, Barry P. Another complication of combined extraduralsubarachnoid technique. Br J Anaesth 1995;75:370–1.
  93. Lhuissier C, Mercier FJ, Dounas M, et al. Sumatriptan: an alternative to epidural blood patch? Anaesthesia 1996;52:1078 –9.
  94. Connelly NR, Parker RK, Rahimi A, Gibson CS. Sumatriptan in patients with postdural puncture headache. Headache 2000;40:316–9.
  95. Digivovanni AJ, Dunbar BS. Epidural injections of autologous blood for post-lumbar puncture headache. Anesth Analg 1970; 49:268 –71.
  96. Olsen KS. Epidural blood patch in the treatment of post-lumbar puncture headache. Pain 1987;30:293–303.
  97. McGruder JM, Cooke JE, Conroy JM, et al. Headache after lumbar puncture: review of the epidural blood patch. South Med J 1988;81:1249 –52.
  98. Heide W, Diener HC. Epidural blood patch reduces the incidence of post lumbar puncture headache. Headache 1990;30:280 –1.
  99. Sandesc D, Lupei MI, Sirbu C, Plavat C, Bedreag O, Vernic C. Conventional treatment or epidural blood patch for the treatment of different etiologies of post dural puncture headache. Acta Anaesthesiol Belg 2005;56:265–9.
  100. Gormley JB. Treatment of post-spinal headache. Anesthesiology 1960;21:565– 6.
  101. Berger CW, Crosby ET, Grodecki W. North American survey of the management of dural puncture occurring during labor epidural analgesia. Can J Anaesth 1998;45:110–4.
  102. Safa-Tisseront V, Thormann F, Malassine P, et al. Effectiveness of epidural blood patch in the management of post-dural puncture headaches. Anesthesiology 2001;95:334 –9.
  103. Abouleish E, Vega S, Blendinger I, et al. Long-term follow-up of epidural blood patch. Anesth Analg 1975;54:459–63.
  104. Taivainen T, Pitkanen M, Tuominen M, et al. Efficacy of epidural blood patch for post dural puncture headache. Acta Anaesthesiol Scand 1993;37:702–5.
  105. Williams E, Fawcett W, Jenkins G. Preventing headache after lumbar puncture: optimism generally quoted for epidural blood patching is unwarranted. Br Med J 1998;317:1588 –9.
  106. Oh J, Camann W. Severe acute meningeal irritative reaction after epidural blood patch. Anesth Analg 1998;87:1139–40.
  107. Sperry RJ, Gartrell A, Johnson JO. Epidural blood patch can cause acute neurologic deterioration. Anesthesiology 1995;82:303–5.
  108. Diaz J. Permanent paraparesis and cauda equine syndrome after epidural blood patch for postdural puncture headache. Anesthesiology 2002;96:1515–7.
  109. Gutterman P, Bezier HS. Prophylaxis of post myelogram headaches. J Neurosurg 1978;49:869 –71.
  110. Colonna-Romano P, Shapiro BE. Unintentional dural puncture and prophylactic epidural blood patch in obstetrics. Anesth Analg 1989;69:522–3.
  111. Loeser EA, Hill GE, Bennett GM, et al. Time versus success rate for epidural blood patch. Anesthesiology 1978;49:147– 8.
  112. Palahnuik RJ, Cumming M. Prophylactic blood patch does not prevent post-lumbar puncture headache. Can Anaesth Soc J 1979; 26:132–3.
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categories: Emergency Medicine

California: Doctors lose discrimination case

by Paul Rega, MD — published on August 19th, 2008

Boston Globe, 8/19/08

http://www.boston.com/news/nation/articles/2008/08/19/top_calif_court_rules_doctors_cant_deny_treatment_to_gays/

Doctors cannot discriminate against gays and lesbians in medical treatment, even if the procedures being sought conflict with physicians’ religious beliefs, the California Supreme Court decided unanimously yesterday.

In the second gay-rights victory this year, the state Supreme Court said religious physicians must obey a state law that bars businesses from discriminating on the basis of sexual orientation.

“The First Amendment’s right to the free exercise of religion does not exempt defendant physicians here from conforming their conduct to the . . . antidiscrimination requirements,” Justice Joyce L. Kennard wrote for the court.

The decision stemmed from a lawsuit filed by Guadalupe T. Benitez, a lesbian who lives with her partner in Oceanside, a coastal city 35 miles north of San Diego, and wanted to become pregnant with donated sperm.

Benitez contended that Dr. Christine Brody, an obstetrician at the North Coast Women’s Care Medical Group, told her that her religious views prevented her from performing an intrauterine insemination on a lesbian.

Another physician at the clinic, Dr. Douglas Fenton, told Benitez that the staff was uncomfortable helping her conceive a child and advised her to find a doctor outside the medical group, Benitez said.

The doctors denied the allegations. Brody said she would not perform the procedure on any unmarried woman, heterosexual or homosexual.

Justice Marvin Baxter, in a separate concurring opinion, said doctors can avoid liability by referring patients who want procedures that conflict with their religion to other physicians in the practice.

A trial court ruled for Benitez, but an appeals court overturned that decision. After the case landed in the state high court, civil libertarian groups sided with Benitez; religious groups, including Jewish rabbis and Islamic clergy, argued that doctors were entitled to disavow treatments that conflicted with their religion.

The ruling was unanimous and a succinct 18 pages, a contrast to the state Supreme Court’s 4-3 split in May legalizing marriage between same-sex couples.

Benitez, 36, and now the mother of three, said she has been pursuing her case for 10 years.

“This isn’t just a win for me personally and for other lesbian women,” she said. “It’s a win for everyone, because anyone could be the next target if doctors are allowed to pick and choose their patients based on religious views about other groups of people.

“It was an awful thing to go through,” Benitez said. “It was very painful – the fact that you have someone telling you they will not help you because of who you are, that they will deny your right to be a mother and have a family.”

Benitez has given birth to three children through artificial insemination – Gabriel, 6, and twin daughters, Sophia and Shane, who turn 3 this weekend.

Jennifer Pizer, Benitez’s attorney, said that the ruling was “a victory for public health” and that she expected it to have nationwide influence.

“It was clear and emphatic that discrimination has no place in doctors’ offices,” Pizer said.

Robert Tyler, general counsel for Advocates for Faith and Freedom, said the decision might be appealed to the US Supreme Court.

He said the ruling would spur voters “to recognize the radical agenda of our opposition” and support a November ballot initiative that would amend the state Constitution to ban same-sex marriage in California.

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categories: Emergency Medicine