Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 911 - файл

.pdf
Скачиваний:
0
Добавлен:
29.08.2026
Размер:
8 Мб
Скачать
406
https://t.me/medicina_free
TABLE56.2 VASCULAR DISTRIBUTION:CRANIAL
Artery Clinical Presentation
to lower placental transmission and decreased association with fetal acidosis.20 Vasopressin receptors (V1) are pres­ent on the human uterus, and administration of vasopres-
Anterior Cerebral Artery
Middle Cerebral Artery
Posterior Cerebral Artery
Lower extremity weakness and sensory
loss:contralateral side Apraxia Speech dysfunction:initiation
Facial, upper and lower extremity weakness and
sensory loss:contralateral side Aphasia:expressive, receptive
Sensory loss:contralateral side Cognitive impairment Visionloss Language dysfunction
sin for hypotension can induce uterine contractions.21 Epinephrine is a suitable third- line agent for treatment of hemodynamic instability. Risk of uterine arterial vaso­constriction is balanced by tocolysis and decreased uterine vascular resistance.
22
Not all molecules cross the placenta, and movement is dependent on hydrostatic, osmotic pressure gradients and concentration gradients. All beta blockers, hydrala­zine, nitroprusside, and nitroglycerin cross the placenta. Beta blockers can cause a transient fetal bradycardia, but
Cerebellar Artery Ataxia
Vision impairment Vertigo Speech impairment Loss of consciousness
Basilar Artery Cranial nerve dysfunction
Ataxia Cognitive impairment Temperature and sensoryloss Motor weakness:contralateral side
NOTE:There is much overlap in presenting signs and this list is not exhaustive.
potential maternal benet from decreasing blood pres­sure or heart rate may outweigh fetal risk. Angiotension­converting enzyme (ACE) inhibitors are contraindicated in the second and third trimesters secondary to teratogenic eects,23 so they are not typically used for maintenance during pregnancy and would not be ideal for acute blood pressure management. Magnesium sulfate is administered to parturients for seizure prophylaxis in preeclampsia and for fetal neuroprotection in prematurity <32 weeks gesta­tional age, and can cause hypotension, uterine atony, and
addition, parturients can present with other signs such as seizures, visual changes, ataxia, weakness, facial drooping, and altered consciousness.19 See Table 56.2. Any concern­ing neurological signs in the parturient should be evaluated immediately, as outcomes seem to be worse in pregnancy.
hypotonia. Parturients who receive mannitol to reduce elevated intracranial pressure (ICP) are at risk for drug accumulation in the fetus, resulting in a hyperosmolar state, reduced urinary blood ow, and lung uid produc­tion.24 All anticonvulsants cross the placenta and have the potential to cause neural tube, orofacial, cardiovascular,
PREGNANCY- SPECIFIC CONSIDERATIONS
and digital malformations, when given early in pregnancy, as well as fetal coagulopathies. Valproate, phenytoin, car­bamazepine, phenobarbital, and topiramate all have been
If the parturient is not postpartum, management of stroke/ intracranial hemorrhage should include consid­eration of uterine blood ow (UBF) to preserve a viable pregnancy. Uterine blood ow is not autoregulated; therefore it is dependent solely on maternal systolic blood pressure and cardiac output. In hypertensive patients, blood pressure should not be dropped too aggressively. Hypovolemia, vasodilators, many anesthesia medications, positive pressure ventilation, sympathetic blockade, aor­tocaval compression, and uterine hypertonicity (due to oxytocin or alpha- adrenergic stimulation), can all cause decreased UBF. If the parturient requires general anesthe­sia for diagnosis or treatment of a neurologic event, exces­sive hyperventilation and hypocapnia should be avoided in order to prevent placental vasoconstriction and fetal compromise. If vasopressors are needed for hypotension following stroke/ intracranial hemorrhage, phenylephrine may be preferred over ephedrine as rst- line therapy due
associated with congenital malformations.25 Levetiracetam (Keppra) is commonly used for seizure prophylaxis follow­ing an intracranial event, and in one recent study from Australia, there were no malformations seen in parturients taking Keppra.26 At term, there is no risk of congenital malformation related to medication, as organogenesis is complete.
Ionizing radiation exposure during diagnostic proce­dures such as CT could result in spontaneous abortion, congenital malformation, or cerebral injury, depending on dose and timing of exposure. Exposure during the rst 15 weeks of development places the fetus at greatest risk for injury, and the risk declines by a factor of 4 aer 15 weeks gestation, likely due to completion of organogenesis. Aer 26 weeks gestation, the risks are minimal. e American College of Obstetricians and Gynecologists recommend that exposure during pregnancy not exceed 5 rad (radia­tion absorbed dose). e parturient should be shielded
406 SECTION D.NEUROLOGICCRISES
https://t.me/medicina_free
407
with lead in the anterior and posterior position during any exposure, to minimize risk. For reference, a computed tomography (CT) of the chest results in fetal exposure of up to 0.1 rad and a chest x- ray results in exposure of <0.001 rad.27 Radiopaque agents used in CT scans can contain iodine and cross the placenta, potentially resulting in fetal hypothyroidism, but these techniques should be used if the maternal benet outweighs the risk to the fetus.28 Contrast is excreted minimally in the breastmilk, and there is no pre­caution regarding lactation for postpartum women. e safety of paramagnetic contrast agents (Gadolinium) has not been established in humans, but they do cross the pla­centa and should be used only if absolutely essential, espe­cially during the rst trimester.
28
blood pressure is maintained.30 However, while it is quite unlikely that general anesthesia would be undertaken for the purposes of blood pressure control, given the associated increase in ICP, it is important to note that MAC is reduced by 30%– 40% in the parturient.
31
e American College of Obstetricians and Gynecologists (ACOG) recommends that any fetus termed viable (approximately 24 weeks) should have at a minimum Doppler fetal heart tones and tocometer analy­sis immediately prior to and aer an operation/ interven­tion.32 Continuous intraoperative monitoring should be performed for a viable fetus during intervention follow­ing maternal stroke/ intracranial hemorrhage if (1) there is an obstetrical physician or nurse qualied to interpret the fetal tracing; (2) monitoring is possible during the
ANESTHETIC CONSIDERATIONS SPECIFIC TOTHE PARTURIENT WITHSTROKE/ INTRACRANIAL BLEEDING
surgery, and (3)an emergency cesarean delivery could be performed without compromising the parturient’s safety. Management and treatment of these parturients should take place in a facility that has obstetrical, pediatric, and neonatal expertise readily available. e operating room
For all procedures requiring general anesthesia, pregnant patients >18– 20 weeks gestation should receive a nonpartic­ulate antacid, an H2 blocker, and a gastric motility agent and a rapid sequence induction (RSI) is recommended. When the gestational age is >20 weeks, le uterine displacement (LUD) should also be maintained. Agents that increase ICP should be avoided (e.g., ketamine), and succinylcholine may produce transient increases in ICP. However, those increases may be abolished with IV lidocaine, adequate depth of anes­thesia, hyperventilation, or a defasciculating dose of a nonde­polarizing paralytic.29 An arterial line should be considered for close blood pressure monitoring and should be main­tained within 20% of baseline, with a mean arterial pressure of >70mmHg. Invasive blood pressure monitoring should also be considered for laboring patients with stroke/ intracra­nial hemorrhage if vasoactive medications are required for tight blood pressure control. A sodium nitroprusside drip can be used to lower blood pressure, but it crosses the pla­centa and may cause fetal cyanide toxicity (keep infusions to less than 0.5 mg/ kg/ h and minimize duration of time on infusion). Nitroglycerin can also be used to control blood pressure without adverse fetal eects, although experimen­tally, nitroglycerin is metabolized to nitrites, causing met­hemoglobinemia and cerebral vasodilation. Nicardipine infusion oers the advantage of easy titration and short duration of action if blood pressure control requires con­tinuous medication administration. Inhalation agents like isourane can also be used to lower blood pressure and even at greater than 1 MAC (minimum alveolar concentration), uteroplacental perfusion is maintained as long as maternal
should be equipped for an emergency cesarean section should the need arise.32 Continuous intraoperative fetal monitoring for a previable fetus should be performed to optimize placental blood ow in cases of fetal bradycardia and on a case- by- case basis.32 Loss of beat- to- beat vari­ability is normal during general anesthesia, but fetal heart rate decelerations are abnormal and should be corrected with increased blood pressure, increased oxygenation, or a change in position.
When a parturient presents in labor with intracranial pathology there are several management concerns depend­ing on the etiology, including acuity, presentation, location, size, and how the pathology has been managed. Amultidis­ciplinary meeting with obstetricians, neurologists, anesthe­siologists, and neonatologists is critical if time permits.
Parturients with history of ischemic stroke presenting in labor are likely anticoagulated, and normalization of coagu­lation values is required before neuraxial analgesia can be provided (refer to American Society of Regional Anesthesia guidelines). ese patients can be managed expectantly and deliver vaginally if there is adequate normotensive blood pressure control. Acesarean section is usually only indicated for obstetric indications, as the surgery itself may be a risk factor for postpartum stroke; tight blood pressure control is paramount. General anesthesia should be induced with care and special attention given to minimize uctuations in hemodynamics.
Parturients with treated, stable intracranial hemor­rhage (embolization of AVM or clipping of aneurysm) can labor, but blood pressure should be well controlled. An
STROKE/SUBARACHNOID HEMORRHAGE 407
408
https://t.me/medicina_free
assisted second stage for vaginal delivery would be consid­ered under dense neuraxial anesthesia and anesthetic goals during both the rst and second stages of labor would cen­ter around avoiding hemodynamic lability due to pain as well as Valsalva maneuvers. If a cesarean section is planned for obstetric reasons, neuraxial anesthesia is an option with blood pressure maintained at baseline. Remember that all intracranial lesions can result in cranial mass eect and eleva­tion in intracranial pressure; this should be considered prior to placing any neuraxial anesthetic. Delivering vaginally has not resulted in increased maternal complications for these corrected lesions.
2
When a parturient presents in labor with an unre­paired AVM or aneurysm, they need to be evaluated on a case- by- case basis. ings to consider are the size and loca­tion of the vascular anomaly, as this will drive the mode of delivery. For some lesions, the patient is still encour­aged to delivery vaginally, with close monitoring, possibly invasive, and an assisted second stage with adequate neur­axial analgesia. During a cesarean delivery, hemodynamics should be closely followed with invasive monitoring and neuraxial or general anesthesia. Studies have shown that there is not a standard preferred method of delivery for these cases, so for most treated and managed conditions discussed here, vaginal delivery will be the mode selected.2 All parturients with existing neuropathology should be closely monitored postpartum, potentially in the neuro intensive careunit.
maintained on warfarin. For pregnancies that are consid­ered lower risk, UFH or LMWH are initiated in the initial trimester and then followed with low- dose aspirin for the remainder of the pregnancy.33 In regard to hemorrhagic stroke, the treatment is usually surgical for decompression and evacuation of the hematoma. However, watchful wait­ing, hemodynamic control, and reversal of any coagulopa­thy are options as well, depending on the severity of the hemorrhage.
In any pregnant or immediately postpartum woman with new neurologic complaints, a timely neurology and/ or neu­rosurgery consult should be obtained (Figures 56.1,56.2,). Imaging studies should be performed based on the neuro­logic symptoms and indication. Fetal exposure to ioniz­ing radiation was discussed earlier and should be weighed against the maternal benet. Noncontrast CT is usually the rst imaging modality to evaluate for cranial hemorrhage, but contrast may be needed to further delineate anatomical structures. Also, MRI and MR venogram may be indicated to evaluate for stroke or for other vascular occlusions, and the use of paramagnetic contrast agents should be weighed against the risk. In addition, cardiac ultrasound should be performed in all suspected embolic events to evaluate for right to le intracardiac communication as the etiology of the event. Basic laboratory studies should be evaluated, including hemoglobin, platelet count, electrolytes, liver function tests, and coagulation studies. Complete workup for thrombophilias should be delayed until 6 weeks postpar­tum when the coagulation factors normalize (protein C and
MANAGEMENT AND TREATMENT
S activity, antithrombinIII).
For thrombotic lesions, the use of intra- arterial throm­bolysis has been used successfully in parturients. In one
Hypertensive disorders are the most common etiologies for stroke and intracranial hemorrhage; therefore man­agement involves aggressive blood pressure control dur­ing pregnancy for prevention. Systolic blood pressure of greater than 160mmHg should be immediately addressed with antihypertensive agents. e most commonly used medications considered safe in pregnancy are labetalol, hydralazine, or nifedipine. e goal is to improve sys­temic blood pressure while maintaining adequate cerebral perfusion pressure. It has been shown that controlling the systolic blood pressure is more important than con­trolling diastolic blood pressure.17 For parturients with ischemic/ thrombotic stroke or CVT, the management is medical therapy. American Heart Association guidelines for parturients are unfractionated heparin (UFH) or low molecular weight heparin (LMWH) through 13 weeks of gestation and restarted at approximately 36 weeks until delivery. From 13 through 36 weeks the parturients can be
study, 10 of 11 women who received thrombolysis injected into their vasculature had no major complications, however one woman died of a major complicating illness. e fetal outcomes were positive, with seven neonates delivering without issue, two therapeutically terminated, one sponta­neous abortion in the parturient with bacterial endocardi­tis, and one demise when the parturient passed away.
34– 36
Intravenous/ arterial tPA (tissue plasminogen activator) has a short half- life (less than 5 minutes), but since it binds to new brin clots, the clinical eect can last for hours. It is a large molecule and thus does not cross the placenta, so fetal teratogenic eects should not be a concern. Pregnancy, operative delivery, or postpartum state are not absolute contraindications to intravenous or intra- arterial throm­bolysis, thrombectomy, or craniotomy.
37– 39
Any parturient who requires management of stroke or cranial hemorrhages should be transferred to a stroke unit or tertiary care unit capable of caring for these patients. See Figure 56.2. Any
408 SECTION D.NEUROLOGICCRISES
Suspected Maternal Stroke/Cranial Hemorrhage
https://t.me/medicina_free
409
Critical Assessment Intervention (10 min):
• Activate Emergency Response/Stroke Team
• Monitor and support hemodynamics: blood pressure control is paramount
• Support airway and provide supplemental oxygen if needed
• Confirm/establish IV access
• Time course of symptoms and brief neurological exam and pertinent medical history
• Check glucose
• Laboratory studies if time permits
• Monitor fetus, but do not delay diagnosis or treatment
Prepare for imaging: CT or MRI of the brain depending on urgency of diagnosis (within 25 min)
Cranial Hemorrhage:
• Consult neurosurgeon/neurologist
• Transfer to higher level of care if indicated
• Continue to stabilize until definitive intervention, including blood pressure control
• Check blood availability
• Prepare operating room if needed
Nonhemorrhage/Stroke:
• Consult neurologist
• If < 4.5 hours: fibrinolytic therapy: rtPA is NOT an absolute contraindicated in pregnancy/postpartum period
• If >4.5 hours: intra-arterial intervention
• Supportive care and blood pressure monitoring
Figur e5 6.2 Maternal stroke/ cranial hemorrhage algorithm.
parturient with a Glasgow Coma Score of less than nine, should have her airway protected, especially prior to transfer.
1
• Consider TTE with bubble study, carotid ultrasound, thrombophilia workup, antiplatelet therapy.
autoregulated and is dependent on maternal blood pressure. Fetal monitoring during diagnostic or therapeutic neu­rological procedures should be used based on gestational age and availability of surgical obstetrical intervention. All
CONCLUSIONS
parturients suspected of stroke or intracranial hemorrhage should be treated at a facility capable of managing these
complex conditions. Parturients are at greater risk of stroke and intracranial hemorrhage in the peripartum period due to the physi­ologic changes of pregnancy and hypercoagulable state of
CASE- BASED LEARNING DISCUSSION
pregnancy. Hypertensive disorders are the most common etiologies for intracranial hemorrhage. Aggressive blood pressure control is critical. Diagnosis and treatment should not be delayed based on pregnancy. All necessary imaging and intervention should be pursued regardless of preg­nancy status for maternal well- being, but precautions and fetal monitoring may be warranted. Maintaining hemo­dynamic stability is critical, as uterine blood ow is not
1. What is your dierential diagnosis? What should be the next steps in management?
2. Would you treat her blood pressure? Which medications would you use, and what would be the endpoint?
3. Would you order any imaging studies? Consult any other medical services?
STROKE/SUBARACHNOID HEMORRHAGE 409
410
https://t.me/medicina_free
4. How would your management change if she were postpartum?
5. e parturient becomes unresponsive and demonstrates seizure activity. What do you do now? What are next rst steps? Has your dierential changed? What if she were immediately postpartum?
6. If operative evacuation of a hemorrhage is warranted, how will you provide anesthesia? What if she has just delivered the neonate?
7. If stroke is suspected, how will you medically manage her? Would you anticoagulate her now versus long­term? If so, with what medication?
REFERENCES
1. Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J,
Kurinczuk JJ, eds., on behalf of MBRRACE- UK. Saving lives, improving mothers’ care— lessons learned to inform future mater­nity care from the UK and Ireland condential enquiries into mater­nal deaths and morbidity 2009– 12. Oxford: National Perinatal Epidemiology Unit, University of Oxford;2014.
2. James AH, Bushnell CD, Jamison MG, Myers ER. Incidence and
risk factors for stroke in pregnancy and the puerperium. Obstetrics and Gynecology. 2005;106:509– 16.
3. Rosamond W, Flegal K, Furie K, et al. Heart disease and
stroke statistics— 2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2008;117:e25– e146.
4. Kuklina EV, Tong X, Bansil P, etal. Trends in pregnancy hospital-
izations that included a stroke in the United States from 1994 to 2007:reasons for concern? Stroke. 2011;42:2564– 70.
5. Bateman BT, Olbrecht VA, Berman MF, etal. Peripartum subarach-
noid hemorrhage: nationwide data and institutional experience. Anesthesiology. 2012;116:324– 33.
6. Dias MS, Sekhar LN. Intracranial hemorrhage from aneurysms and
arteriovenous malformations during pregnancy and the puerperium. Neurosurgery. 1990;27:855– 65.
7. Stam J. rombosis of the cerebral veins and sinuses. New England
Journal of Medicine. 2005;352:1791– 8.
8. Moodley J. Maternal deaths due to hypertensive disorders in
pregnancy: best practice and research. Clinical Obstetrics and Gynaecology. 2008;22:559– 67.
9. Tuluc M, Brown D, Goldman B. Lethal vertebral artery dissection
in pregnancy:a case report and review of the literature. Archives of Pathology and Laboratory Medicine. 2006;130:533– 5.
10. Lund CJ, Donovan JC. Blood volume during pregnancy. Signicance
of plasma and red cell volumes. American journal of obstetrics and gynecology. 1967;98:394– 403.
11. Pritchard JA. Changes in the blood volume during pregnancy and
delivery. Anesthesiology. 1965;26:393– 9.
12. Bamber JH, Dresner M. Aortocaval compression in pregnancy:the
eect of changing the degree and direction of lateral tilt on maternal cardiac output. Anesthesia and Analgesia. 2003;97:256– 8.
13. McClelland SH, Bogod DG, Hardman JG. Apnoea in preg-
nancy:an investigation using physiological modelling. Anaesthesia. 2008;63:264– 9.
14. Stirling Y, Woolf L, North WR, etal. Haemostasis in normal preg­nancy. rombosis and Haemostasis. 1984;52:176– 82.
15. Lanska DJ, Kryscio RJ. Risk factors for peripartum and postpar­tum stroke and intracranial venous thrombosis. Stroke. 2000; 31:1274– 82.
16. Bushnell CD, Jamison M, James AH. Migraines during pregnancy linked to stroke and vascular diseases: US population based case­control study. BMJ. 2009;338:b664.
17. Martin JN Jr, igpen BD, Moore RC, etal. Stroke and severe pre­eclampsia and eclampsia:a paradigm shi focusing on systolic blood pressure. Obstet Gynecol. 2005;105:246– 54.
18. Kittner SJ, Stern BJ, Feeser BR, et al. Pregnancy and the risk of stroke. N Engl J Med. 1996;335:768– 74.
19. Crovettoa FB, Somiglianaa EC, Peguerob A, Figueras FB. Stroke during pregnancy and pre- eclampsia. Curr Opin Obstet Gynecol. 2013;25:425– 32.
20. Ngan Kee WD, Khaw KS, Tan PE, etal. Placental transfer and fetal metabolic eects of phenylephrine and ephedrine dur­ing spinal anesthesia for cesarean delivery. Anesthesiology. 2009;111:506– 12.
21. Maggi M, Del Carlo P, Fantoni G, etal. Human myometrium dur­ing pregnancy contains and responds to V1 vasopressin receptors as well as oxytocin receptors. Journal of Clinical Endocrinology and Metabolism. 1990;70:1142– 54.
22. Segal S, Csavoy AN, Datta S. e tocolytic eect of catechol­amines in the gravid rat uterus. Anesthesia and Analgesia. 1998;87:864– 9.
23. Cooper WO, Hernandez- Diaz S, Arbogast PG, etal. Major congen­ital malformations aer rst- trimester exposure to ACE inhibitors. New England Journal of Medicine. 2006;354:2443– 51.
24. Tuncali B, Aksun M, Katircioglu K, etal. Intraoperative fetal heart rate monitoring during emergency neurosurgery in a parturient. Journal of Anesthesia. 2006;20:40– 43.
25. Werler MM, Ahrens KA, Bosco JL, etal. Use of antiepileptic medi­cations in pregnancy in relation to risks of birth defects. Annals of Epidemiology. 2011;21:842– 50.
26. Vajda FJ, Graham J, Roten A, et al. Teratogenicity of the newer antiepileptic drugs— the Australian experience. Journal of Clinical Neuroscience. 2012;19:57– 59.
27. Groen RS, Bae JY, Lim KJ. Fear of the unknown: ionizing radia­tion exposure during pregnancy. American Journal of Obstetrics and Gynecology. 2012;206:456– 62.
28. ACOG Committee Opinion. Number 299, September 2004 (replaces No. 158, September 1995). Guidelines for diagnos­tic imaging during pregnancy. Obstetrics and Gynecology. 2004;104:647– 51.
29. Kovarik WD, Mayberg TS, Lam AM, et al. Succinylcholine does not change intracranial pressure, cerebral blood ow velocity, or the electroencephalogram in patients with neurologic injury. Anesthesia and Analgesia. 1994;78:469– 73.
30. Dahlgren G, Tornberg DC, Pregner K, et al. Four cases of the ex utero intrapartum treatment (EXIT) procedure: anesthetic implications. International Journal of Obstetric Anesthesia. 2004;13:178– 82.
31. Chan MT, Mainland P, Gin T. Minimum alveolar concentra­tion of halothane and enurane are decreased in early pregnancy. Anesthesiology. 1996;85:782– 6.
32. ACOG Committee Opinion No. 474:Nonobstetric surgery during pregnancy. Obstetrics and Gynecology. 2011;117:420– 21.
33. Sacco RL, Adams R, Albers G, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack:a statement for healthcare professionals from the American Heart Association/ American Stroke Association Council on Stroke:co- sponsored by the Council on Cardiovascular Radiology and Intervention:the American Academy of Neurology arms the value of this guideline. Stroke. 2006;37:577– 617.
410 SECTION D.NEUROLOGICCRISES
https://t.me/medicina_free
411
34. Johnson DM, Kramer DC, Cohen E, etal. rombolytic therapy for acute stroke in late pregnancy with intra- arterial recombinant tissue plasminogen activator. Stroke. 2005;36(6):e53– 55.
35. Wiese KM, Talkad A, Mathews M, Wang D. Intravenous recombi­nant tissue plasminogen activator in a pregnant woman with cardio­embolic stroke. Stroke. 2006;37(8):2168– 9.
36. Leonhardt G, Gaul C, Nietsch HH, etal. rombotic therapy in pregnancy. J romb rombolysis. 2006;21(3):271– 6.
37. Murugappan A, Coplin WM, Al- Sadat AN, et al. rombolytic therapy of acute ischemic stroke during pregnancy. Neurology. 2006;66(5):768– 70.
38. Del Zotto E, Giossi A, Volonghi I, etal. Ischemic stroke during preg­nancy and puerperium. Stroke Res Treat. 2011;2011:606– 780.
39. Dapprich M, Boessenecker W. Fibrinolysis with alteplase in a preg­nant women with stroke. Cerebrovasc Dis. 2002;13(4):290.
STROKE/SUBARACHNOID HEMORRHAGE 411
412
https://t.me/medicina_free
57.
POST– DURAL PUNCTURE HEADACHE
PhilipRubin
CLINICALCASE
Whitacre, or other “pencil-point” needles, are associated
with signicantly higher rates of PDPH due to the charac­A 27- year- old female, G2P1, at 6cm dilation, with a body mass index (BMI) of 36, requests an epidural for labor anal­gesia. An anesthesia resident attempts placement with a 17 gauge Tuohy needle, using a loss of resistance to air tech­nique. During needle advancement, the resident notices the syringe suddenly lling with clear uid. e syringe is detached, and free- owing cerebrospinal uid (CSF) pours from the Tuohy needle.
teristics of the dural puncture that they create (cutting the
dura/arachnoid perpendicularly, rather than spreading
bers laterally), which fosters increased CSF ow across
the dura and delayed dural healing.3 Cutting needles have
thus largely fallen out of favor for practitioners performing
neuraxial techniques due to the increased risk for PDPH.
Needle orientation during dural puncture may also con-
tribute to PDPH risk because the dura mater/arachnoid
is composed of collagen bers running longitudinally
RISK FACTORS FORPOST– DURAL PUNCTURE HEADACHE
along the spinal column. Orientation of the needle bevel
parallel to these bers may favor a more “natural” separa-
tion, given the tendency to spread the bers laterally. is
less traumatic insult to the dura may consequently heal Trespass of the dural membrane can be intentional, as with spinal anesthesia or lumbar puncture, or accidental, during the course of other neuraxial procedures or spine surgery. e case above describes an episode of epidural placement, complicated by unintentional dural puncture (UDP) with the Tuohy needle, also known as a “wet tap.” ough rarely a dangerous event, it is commonly accompanied by a mod­erate to severe postural headache, which causes signicant morbidity for the patient.
1
Post– dural puncture headache (PDPH) is more com­mon (>70% risk within 48 hours) aer documented dural puncture with free- owing CSF via a large bore 17– 18 gauge Tuohy needle. Post– dural puncture headache may also occur when dural puncture is intentional, as with spinal anesthesia (22– 27 gauge) or lumbar puncture for CSF evaluation (20– 24 gauge).2 e incidence of PDPH is 1.5% for all epidural placements,3 and approximately 1% for spinal anesthesia using small bore spinal needles.1 e risk increases dramatically with increasing needle size, however some procedures (lumbar puncture) require dural puncture with larger bore needles to draw CSF and meas­ure opening pressure.
Post–dural puncture headache risk also varies by the distinguishing features of dierent needle designs. Quincke or other “cutting” spinal needles, compared with
more quickly, thereby minimizing continued CSF loss. Conversely, a perpendicularly oriented needle bevel may cause more trauma as it cuts through the bers.1 erefore, some providers advocate Tuohy needle advancement in a parallel orientation before entering the epidural space, in case of accidental dural puncture (ADP).
Non- needle- related PDPH risk factors include young age (18– 30), history of headache (HA) prior to dural punc­ture, and low BMI.1 While female gender is not considered an independent risk factor, the incidence is traditionally higher in females because a large percentage (60% incidence in the United States) elect for neuraxial labor analgesia, which incorporates the use of Tuohy needles, increasing the risk of UDP with a large needle. Laboring patients are par­ticularly at increased risk when epidurals are placed at cervi­cal dilation 7 cm, in the lateral decubitus position, or aer multiple attempts or punctures (as in patients with elevated BMI). ese scenarios are commonly associated with more dicult placement and consequently, an elevated risk of UDP during prolonged procedural eorts.4 ough UDP increases with elevated BMI (e.g., >30), actual PDPH inci­dence is lower in this patient population, compared with their nonobese counterparts, likely because of decreased CSF leakage across the dural puncture. is is attributed to increased intra-abdominal pressure in obese patients, which
412
https://t.me/medicina_free
413
increases CSF pressure, while decreasing the size of the epi­dural space, favoring less CSF leakage, yielding a protective eect against development of PDPH.
SYMPTOMS/ PATHOPHYSIOLOGY
5
TABLE57.1 POST– DURAL PUNCTURE HEADACHE
DIFFERENTIAL DIAGNOSIS
Migraine Caffeine Withdrawal
Cluster headache Dehydration
Tension headache Meningitis
Sleep deprivation Cortical vein thrombosis
A postural HA is the sine qua non of a PDPH; it improves when supine, or with the head reclined, and worsens with the head elevated, or when sitting or standing. e HA typ-
Pneumocephalus Subarachnoid hemorrhage
Severe preeclampsia Stress/ anxiety
ically presents in the frontotemporal or occipital areas, and usually develops between 1 and 7days aer dural puncture, distinguishing it from other causes of postpartum HA. ere is no associated aura, although the pain may radi­ate to the neck, causing neck stiness, and the HA may be accompanied by auditory (tinnitus) and visual (diplopia) changes, vertigo, dizziness, nausea, vomiting, and rarely cra­nial nerve palsies.
6,7
e severity of the HA directly correlates with the degree of intracranial hypotension due to the volume of CSF that ows from the intrathecal space into the epi­dural space. Normal CSF pressure in the lumbar region is between 5 and 15cmH20 in the supine position, compared to 40cmH20 when erect. e CSF “loss,” and the resultant CSF pressure in the intrathecal space, are inversely pro­portional. Pressure in the lumbar region may decrease to 4cmH20 or less when recumbent,6, and the drop is eventu­ally transmitted both cephalad and caudad, across the entire spinalcanal.
As one of the roles of CSF is to mechanically support central nervous system (CNS) structures, its reduction in the cranium causes tugging or sagging of the meninges, especially when sitting or standing (due to the addition of gravity’s eect in this position). e resultant traction of these pain- sensitive intracranial structures is the mechanism behind the HA following dural puncture. Upon return to the recumbent position, the HA quickly improves, or even completely disappears due to equalization of CSF pres-
e dierential diagnosis of postpartum HA is quite extensive (Table 57.1), especially for parturients who received neuraxial anesthesia. In fact, 40% of women expe­rience symptoms of HA unrelated to dural puncture aer delivery. ese etiologies include, but are not limited to, dehydration, exhaustion from labor contractions, sleep dep­rivation, caeine withdrawal, stress, musculoskeletal ten­sion, pain, anxiety, and preexisting HA conditions such as migraines.
1,7
For this reason, PDPH is a diagnosis of exclu­sion, and practitioners commonly wait 24 hours postdural puncture prior to labeling a HA meeting the pathogno­monic characteristics of PDPH.
Patients attest to the uniqueness of a PDPH, which they nd debilitating, especially for parturients in the post­partum period. Not only do these patients need to care for themselves and ambulate frequently to minimize the risk of deep vein thrombosis (DVT), but they must also care for their newborn, which requires frequent sitting up and get­ting out of bed. us, unrecognized or inadequately treated PDPH inevitably increases healthcare costs caused by delayed discharge or readmission, and the resultant adjust­ment in nursing ratios that may be necessary to provide additional attention to both mother and baby. Persistent PDPH may also be associated with delayed mother-infant bonding and associated breastfeeding success, which may further increase time to discharge.
8
sure throughout the cranium and spinal canal, and relief of intracranial hypotension.
Since the sum of all structures (brain, CSF, blood vol­ume) in the cranium remains constant, according to the Monro- Kellie doctrine, the loss of CSF volume surround­ing the brain leads to compensatory cerebral venodilation. is results in increased cerebral blood volume, which is another contributing factor to the development of PDPH.6 Movements that commonly prevent cerebral venous drain­age, such as coughing, sneezing, and straining, may further exacerbate HA symptoms.
6
TREATMENT
When a “wet tap” is recognized during epidural placement, the provider has two immediate options: completely with­draw the needle and repeat the procedure, or thread the epidural catheter into the intrathecal space via the Tuohy needle.9 While the former choice is more common, spi­nal catheters have several advantages in this setting. First and foremost, continuous spinal anesthesia is quite relia­ble due to the uniformity of the subarachnoid space. is
POST–DURAL PUNCTURE HEADACHE 413
414
https://t.me/medicina_free
technique may be in the patient’s best interest, especially if epidural placement was dicult, or if the patient had been deemed high risk for requiring cesarean delivery. Special safety measures must be implemented, however, to ensure that the catheter is not inappropriately managed as an epi­dural catheter, as this would place the patient at severe risk for a high spinal.
Interestingly, another potential advantage of threading a spinal catheter is to reduce the risk or severity of PDPH. Several studies have validated this practice, postulating that leaving the catheter in- situ for at least 24 hours aids in the dural healing process. e catheter purportedly induces an inammatory reaction that begins to seal the dural bers around the catheter.9 Other researchers, however, discour­age this practice, claiming either that it adds no clini­cal benet because the CSF pressure gradient is too high immediately aer the puncture to prevent leakage, or that the inammatory process can be disrupted or completely dislodged when the catheter is eventually removed.10 ere still is no consensus on whether to thread or not to thread; the topic continues to be debated and evaluated within the obstetric anesthesia community. Whichever decision is made, however, needs to be consistent with hospital policy, and its sta ’s ability to safely care for the patient by prevent­ing misuse of the catheter. Aggressive labeling is essential to avoid injection of medications intended for the epidural space or intravenous route. Repeated access of an intrathe­cal catheter should be limited, as each manipulation can place the patient at increased risk for CNS infection.
Management of PDPH varies dependent on severity, but conservative measures that oer symptomatic relief are traditionally implemented rst (Box 57.1). Approximately 150 mL of CSF is produced daily, compared with the aver­age total CSF volume in the spinal canal and cranium of 500 mL. Since CSF continues to leak at a rate faster than new CSF production, patients are instructed to hydrate aggressively, as this may promote increased CSF production to replenish the “lost” volume. Increased production theo­retically helps to increase intrathecal CSF pressure, coun­teracting the pressure reduction caused by CSF leakage.6 If
BOX 57.1 CONSERVATIVE PDPH TREATMENTS
Hydration (oralorIV)
Analgesics (oralorIV)
Caffeine (oralorIV)
Rest/ recumbency
a patient has diculty consuming large amounts of uids, then increasing intravenous uids is a viable alternative in admitted patients.
Initiation of multimodal analgesia is also benecial; patients are encouraged to routinely request their “as needed” medications for postpartum pain around the clock. Such medications (in both oral and intravenous form) usu­ally include opioids, nonsteroidal anti- inammatory drugs (NSAIDS) such as ketorolac and ibuprofen, and also acet­aminophen.11 While they may aid in attenuating PDPH, unfortunately some (especially opioids) commonly cause untoward side eects including nausea, vomiting, and pru­ritis. us the utility of oral and intravenous analgesics is sometimes limited in the treatment of PDPH, because patients may choose to discontinue opioids altogether. Other studied treatments that have proven to be of mixed success include pregabalin, gabapentin, sumatriptan, and ACTH (cosyntropin).11 Unfortunately, relying solely on these anal­gesic varieties oen does not reliably oer substantial relief to ultimately improve patient mobility and function.
Caeine intake is another conservative treatment for PDPH, because it acts as a potent cerebrovascular vasocon­strictor via its inhibition of adenosine receptors. Caeine crosses the blood- brain barrier, and ultimately decreases cerebral blood ow, counteracting the cerebral vasodilation that has occurred due to CSF loss. Patients are encouraged to consume beverages high in caeine (e.g., coee and soda) in large quantities.1 Alternatively, providers may prescribe intravenous (IV) caeine or oral formulations, which are commonly combined in commercial preparations with bar­biturates along with either acetaminophen or aspirin, such as Fioricet and Fiorinal, respectively. ough sometimes initially helpful, caeine’s ultimate benet is limited since its eect is not sustained.
6
Rest is sometimes recommended to patients with PDPH, though evidence supporting faster recovery or prevention is limited.1 By remaining supine, or avoiding postural changes in another reclined position, the HA can be minimized as CSF pressure remains relatively uniform throughout the cranium and spinal canal in the recumbent position. e feasibility of this treatment, while acceptable to some, is not realistic for parturients in the immediate postpartum period due to the demands of caring for a new­born. Even with assistance, PDPH is oen too debilitating for any meaningful participation at all. Additionally, con­nement to a bed in the supine position for extended peri­ods of time increases the risk of DVT in patients already hypercoagulable from pregnancy.
While conservative management may help temporize symptoms of PDPH, they remain as advertised:conservative.
414 SECTION D.NEUROLOGICCRISES
https://t.me/medicina_free
415
Some patients benet and the HA improves to a managea­ble level (especially those with smaller holes caused by spi­nal needles), but unfortunately they may end up discharged with the ability to care for neither themselves nor their newborn at home due to sustained CSF leakage. Usually PDPH is a self- limiting process, with complete resolution in 7– 10 days. Via broblastic proliferation from the sur­rounding tissue, and blood clot at the puncture site, 85% of PDPH cases eventually resolve on their own within 6 weeks.6 However, this can be an unbearable amount of time for a patient to cope with debilitating HA symptoms.
Some patients receiving an EBP do not present with IV access, either due to proximity to discharge or because they return as outpatients. It is important to follow institutional policy for monitoring during the procedure, which usually includes blood pressure and pulse oximetry (with heart rate) monitoring. Even though medications are not being administered via an epidural catheter during EBP, IV access is essential, since the patient may still experience hemody­namic changes during the procedure (i.e., vagal responses), requiring intervention with uids and vasopressors.
Informed consent is vital prior to EBP, since it car­ries the same risks as with any epidural placement, which
EPIDURAL BLOODPATCH
Since many PDPH do not rapidly improve with conserva­tive measures, many patients elect for the more invasive, “gold standard” treatment for PDPH: epidural blood patch (EBP). e EBP is the denitive treatment for PDPH, because it directly confronts the cause (CSF leak­age from the intrathecal space). e treatment was origi­nally devised from a casual observation that bloody “wet taps” were associated with a reduction of PDPH, since in these cases, autologous coagulation factors were intro­duced into the epidural space.6 e procedure requires two providers, one to draw the patient’s blood (commonly from the hand or arm), and the other to place a Tuohy needle into the epidural space, both under sterile condi­tions. e patient may be placed in the sitting or lateral position, but some providers prefer the lateral position, because this oers the patient additional comfort by min­imizing PDPH symptoms for extended periods of time during the procedure.
If indicated, many clinicians wait at least 24 hours post ADP to diagnose PDPH, and perform an EBP. However, some clinicians advocate prophylactic EBP at just 5 hours or more aer nal epidural anesthetic dosing. is is accomplished via injection of autologous blood through an in- dwelling epidural catheter before it is eventually pulled. While the benet of this practice is controversial, one recent study documented decreased PDPH rates using this strategy, when compared with therapeutic EBP aer 24 hours.12 Others claim, however, that prophylactic EBP does not lead to decreased incidence of PDPH. ey fur­ther purport that even in the presence of classic PDPH symptoms early on, EBP are not as eective in completely resolving PDPH, compared with therapeutic EBP aer 48
13,14
hours.
is may be partially due to misdiagnosis, or due to sustained CSF pressure gradients across the dura shortly aer ADP, that may either hinder clot formation, or pro­mote clot dislodgement.
includes bleeding, infection, nerve injury, and of course worsened PDPH due the possibility of a repeat ADP. is risk is likely increased if an experienced provider deemed the initial placement dicult. Patients should also be screened for HA due to postpartum preeclampsia, and if blood pres­sure is signicantly elevated, the obstetric team should be notied to evaluate the patient prior to EBP. Patients with a history of thrombocytopenia or other hematologic dis­turbances should undergo laboratory analysis prior to pro­ceeding with EBP.
Needle entry may occur at the same level as the origi­nal epidural placement or above or below this level. Since it is oen impossible to determine whether an epidural was truly “dicult” at that level, or whether the dural puncture occurred due to inexperience, many providers advocate performing EBP above or below the original site. Since two- thirds of any epidural space injectate typically travels cephalad, it may be benecial to perform the EBP below the level of the puncture, in order to maximize blood and clotting factor exposure at the dural puncture site. Loss of resistance (LOR) to saline should be used, as LOR to air increases the risk of pneumocephalus and its associated HA, given the known dural puncture. When LOR is posi­tive as the Tuohy needle enters the epidural space, the sec­ond provider should draw the patient’s blood separate from the intravenous line under sterile conditions. e blood is then slowly injected into the epidural space via the Tuohy needle. Injection should immediately cease if the patient experiences severe back pain (not simply pressure), or when up to 20– 30 mL of blood has been administered, which­ever comes rst.15 e Tuohy needle is then removed, and the procedure is complete.
Oen, PDPH resolves completely within the rst hour of the procedure. ere are two predominant the­ories that postulate how an EBP works. In the rst, the volume introduced is that the volume introduced into the epidural space increases pressure in that area, decreas­ing the pressure gradient across the dura, which in turn
POST–DURAL PUNCTURE HEADACHE 415
Соседние файлы в папке @xirurgi_2025