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Case Study #2 SOAP Note
Lisa
Case 8-2009 — A 36-Year-Old Woman with Headache, Hypertension, and Seizure 2 Weeks Post Partum.
Aneesh B. Singhal, W. Taylor Kimberly, Pamela W. Schaefer, E. Tessa Hedley-Whyte
The New England Journal of Medicine, Volume 360, Issue 11, Pages 1126 - 1137, 12 March 2009.
https://www-nejm-org.libproxy.uccs.edu/doi/pdf/10.1056%2FNEJMcpc0809063
S
: 36 y/o female 19 days postpartum admitted to Massachusetts General Hospital due to headaches,
hypertension, and seizures. Pt delivered healthy twins at 35.6 weeks gestation via cesarean section for breech
presentation at another hospital without complications during pregnancy.
Brief associated medical history leading up to current admission to Mass Gen Hospital
:
5 days postpartum
: Pt was discharged.
10 days postpartum
: Pt c/o intermittent, throbbing, bifrontal HA.
12 days postpartum
: Pt saw her gynecologist with continued headaches with pain 8/10 and B/P
150/72; pt referred to internist the same day. Pt stated her HA resolved in waiting room of internal
medicine clinic and went home without being seen. Pt reported to a different ER that evening c/o
recurring HA. B/P was 190/80, CT and MRI of brain and laboratory testing did not show any significant
findings. Pt administered oxycodone-acetaminophen for pain and discharged after B/P decreased to
168/70.
15 days postpartum
: Pt saw internist c/o sudden onset HA’s that woke her from sleep early in the
morning and in the late afternoons. Pt reported current HA in office as dull with pain 2/10; B/P 142/78.
Trace peripheral edema present with rest of exam having normal results. Pt Rx furosemide and
potassium chloride.
17 days postpartum
: Pt returned to ER c/o severe HA with nausea, photophobia, and pain 10/10, B/P
204/96. Lab report showed complete blood count was normal other than hematocrit 34.7%. Additional
normal Labs: serum electrolytes, magnesium, calcium, phosphorus, LFT and RFT. UA results = specific
gravity 1.020, pH 6.0, protein 30 mg/dL, and 5-10 RBC. Shortly after IV hydromorphone was given, a
generalized tonic-clonic seizure occurred with urinary incontinence and LOC x2 min. CT of head was
normal. CSF lab results showed no cells, elevated protein level (64 mg/dL), low glucose level (54
mg/dL), and Gram staining and culture were negative. IV metoclopramide, lorazepam, and fentanyl
given and oral oxycodone and methyldopa given; pt reported persistent frontal HA with pain 4/10. SBP
ranged from 140-160. Continuous IV infusion of magnesium sulfate and hydralazine give, pt transferred
from ER to ICU.
18 days postpartum
: MRI with MRA and venography showed posterior white-matter changes on T
2
-
weighted sequences and multifocal narrowing and dilatation of all the intracranial arteries.
o
Brain MRI showed hyperintense regions involving the posterior parietal–occipital lobes, the left
frontal cortex, and the subcortical white matter. These areas had increased diffusion, indicating
vasogenic edema.
o
MRA of circle of Willis showed multifocal stenoses in the proximal anterior, middle, and posterior
cerebral arteries.
19 days postpartum
: pt appeared confused with episode of difficulty word-finding and pronunciation x5
min and right hemiparesis. Aspirin administered. CT scan showed no acute infarction or hemorrhage
evidence. Pt transferred to Mass Gen Hospital via ambulance, arriving 4 hours after aphasia episode.
Current Medication prior to admission
: furosemide, iron, multivitamins, oxycodone-acetaminophen. No oral
contraceptives. NKDA.
Social Hx
: Pt lives with husband and their 3 children (2 y/o child and 19-day old twins).
Tobacco
: denies use.
ETOH
: denies use.
Recreational
: denies use.
PMHx
: no HTN, HA’s, or exlampsia prior to or during pregnancies. Normal routine prenatal screening.
FMHx
: Mother – HTN. Father – cardiovascular disease. No eclampsia
O
:
Vital Signs
on Admission to Mass Gen 19 days postpartum:
Temp
: 36.8°C,
B/P
: 136/91 mmHg,
HR
: 95 bpm,
RR
: 24 bpm,
SpO2
: 98% ambient air, G3P3.
Physical Examination Findings
:
19 days postpartum (day 1 Neuro ICU
):
o
Peripheral edema (1+), normal general physical examination.
o
SBP ranged from 110 to 120 mmHg.
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Case Study #2 SOAP Note
Lisa
Neurological Examination
:
19 days postpartum (PRIOR to Neuro ICU admission
):
o
Pt’s speech was fluent and clear, but responses were slow. The first cranial nerve was not
tested; other cranial nerves were normal. Strength 4/5 on right, normal on left. Ataxia noted
during
rapid alternating movements and finger-to-nose and heel–knee–shin testing; pt was not
able to touch her nose with her right forefinger. Gait was not tested. The remainder of the
neurologic examination was normal.
19 days postpartum (AFTER admitted to Neuro ICU, day 1
):
o
Pt’s level of alertness fluctuated and there was intermittent right hemiparesis.
20 days postpartum (day 2 Neuro ICU
):
o
During the day, pt developed weakness in the right arm and both legs, and LOC decreased. Pt
did not seem to track gaze but moved her fingers on command, withdrew arms and legs on
stimulation, and occasionally answered questions. At times she was unresponsive, with her
eyes open.
21 days postpartum (day 3 Neuro ICU)
:
o
neurologic deterioration noted with unresponsiveness, continuous lip smacking and chewing
movements, and spasticity and hyperreflexia in all limbs, with extensor plantar responses.
26 days postpartum (day 7 Neuro ICU
):
o
pupils were dilated and did not react to light.
Rx given
after admission to Mass Gen Neuro ICU
:
Subsequent days postpartum (day 2-7 Neuro ICU
):
o
IV fosphenytoin, labetalol, and magnesium sulfate given via continuous infusion.
o
Nicardipine was injected into the left vertebral and right and left internal carotid arteries,
resulting in nearly complete resolution of the arterial narrowing.
o
Nimodipine was administered. Repeated cerebral angiography with the administration of
intraarterial and intravenous nicardipine again resulted in improvement of the arterial narrowing.
Treatment with intrathecal nicardipine, insulin on a sliding scale, cefazolin, nafcillin, propofol
(titrated to intracranial pressure) and milrinone was begun.
o
intravenous phenylephrine, fludrocortisone, and intravenous norepinephrine were administered
in an effort to raise systemic blood pressure and improve cerebral perfusion.
o
Hypertonic therapy, mannitol, pentobarbital, acetylcysteine, and hypothermia were
administered, but the patient's condition did not improve.
Laboratory Testing
:
19 days postpartum (day 1 Neuro ICU
):
o
D-dimer level = 1975 ng/mL (normal level <500)
o
CBC = normal
o
serum electrolytes, calcium, phosphorus, and magnesium = normal.
o
RFT and LFT = normal.
20 days postpartum (day 2 Neuro ICU
):
o
plasma triglyceride level = 168 mg/dL (reference range 40-150 mg/dL)
o
anticardiolipin IgM antibody level = 17.9 IgM phospholipid units (reference range 0-15)
o
erythrocyte sed rate = 51 mm/hr (reference value <25)
o
lipids, creatine kinase, troponin T, thyrotropin, & complement (C3 and C4) = normal
o
negative test results for antibodies to proteinase 3, antibodies to myeloperoxidase,
antineutrophil cytoplasmic antibodies, anticardiolipin IgG antibodies, antinuclear antibodies, and
rheumatoid factor.
Radiological Report
:
19 days postpartum (day 1 Neuro ICU
):
o
follow-up MRI showed the expansion of the previously abnormal hypertense regions with new
restricted diffusion, indicating cytotoxic edema secondary to ischemia.
o
MRA showed worsening of the parenchymal lesions and worsening of the multifocal anterior,
middle, and posterior cerebral-artery stenoses.
20 days postpartum (day 2 Neuro ICU
):
o
CT angiographic showed presence of multifocal severe proximal stenoses of the anterior,
middle, and posterior cerebral arteries.
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Case Study #2 SOAP Note
Lisa
21 days postpartum (day 3 Neuro ICU)
:
o
digital-subtraction angiogram showed severe segmental narrowing and dilatation of multiple
intracranial arteries in the anterior, middle, and posterior vascular territories.
22 days postpartum (day 4 Neuro ICU
):
o
Head CT scans and CT angiographic images showed recurrent severe narrowing of the distal
branches of the left middle cerebral artery and both posterior cerebral arteries, with increased
mean transit times of blood through both posterior and distal territories of the middle cerebral
artery.
o
Transcranial Doppler study showed increased blood-flow velocities consistent with the presence
of severe right and mild left vasospasm.
o
After nimodipine administered, Repeated cerebral angiography with the administration of
intraarterial and intravenous nicardipine again resulted in improvement of the arterial narrowing.
Next 24 hours, 23-24 days postpartum (days 4-5 Neuro ICU
):
o
Transcranial Doppler studies showed continuing vasospasm.
o
Head CT scan revealed progressive watershed-territory infarctions with extensive cerebral
edema.
25 days postpartum (day 6 Neuro ICU
):
o
MRI showed extensive ischemia and edema in both cerebral hemispheres.
26 days postpartum (day 7 Neuro ICU
):
o
Final brain MRI showed infarctions in brain stem, bilateral thalami, and bilateral frontal, parietal,
and occipital lobes, with hemorrhagic transformation in some regions of ischemia, diffuse brain
swelling with effacement of the basilar cisterns, and transtentorial herniation.
Electroencephalography Results
:
19 days postpartum (day 1 Neuro ICU
):
o
Portable equipment showed no abnormalities.
20 days postpartum (day 2 Neuro ICU
):
o
Continuous EEG monitoring showed intermittent slowing of delta and theta waves bilaterally,
intermittent low-amplitude beta activity bilaterally, and no epileptiform discharges.
Pathological Findings
:
Postmortem examination was restricted to the brain which was swollen and soft, weighing 1504g
(normal range 1250-1400). It showed widespread recent infarction, diffuse neuronal necrosis, and small
vessel changes suggestive of early hypertensive vascular changes.
The small blood vessels in the white matter had scattered hemosiderin-laden macrophages in their
adventitia, a feature suggestive of early hypertensive vascular changes. The arteries of the circle of
Willis appeared normal, except for one patch of subendothelial thickening in the posterior cerebral
artery.
Coronal sectioning revealed a dusky cut surface with a blurred junction of gray and white matter,
particularly in the border-zone areas. A hemorrhage in the right frontal and parietal lobes, related to the
ventricular drain track, extended across the midline into the left frontal lobe. The lateral ventricles were
mildly dilated and contained a blood clot. On microscopical examination, there was widespread recent
infarction, approximately 48 to 72 hours old, with foci of hemorrhage consistent with reperfusion. There
was diffuse neuronal necrosis secondary to hypoxic–ischemic injury.
No specific morphologic abnormalities corresponding to diffuse vascular spasm were identified.
Blood levels of placental growth factor (PlGF) and a soluble PlGF receptor (sFlt-1, members of the
vascular endothelial growth factor [VEGF] pathway) and a soluble form of the transforming growth
factor β1 receptor (soluble endoglin) correlate with the presence of antepartum eclampsia and also
predict its development. Plasma from the patient was analyzed in the laboratory of Dr. Ravi Thadhani at
this hospital. We compared the results in this patient with the mean values reported in the literature for
antepartum and postpartum patients. This patient had a slightly elevated sFlt-1 level (121 pg per
milliliter) but virtually no PlGF (<5 pg per milliliter) in her serum. Since sFlt-1 is an antiangiogenic factor
that acts by binding the proangiogenic protein PlGF, the relative levels of these proteins may predict
their functional status better than absolute levels. The sFlt-1:PlGF ratio is a better predictor of
antepartum preeclampsia than the absolute levels, especially when the ratio is above 5. This patient's
sFlt-1:PlGF ratio of 24.2 approaches the mean ratio of approximately 32 in patients with antepartum
preeclampsia. These data suggest that a functionally low PlGF state, similar to that seen in antepartum
preeclampsia, may have played a role in this patient's disease process.
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Case Study #2 SOAP Note
Lisa
A
: The patient's condition is consistent with delayed postpartum eclampsia with postpartum angiopathy
(reversible cerebral vasoconstriction syndrome) complicated by brain edema and ischemic and hemorrhagic
strokes. The clinical presentation and imaging findings suggest a dynamic process of arterial vasoconstriction.
Initial Diagnosis
: Recurrent headaches with hypertension developed in this 36-year-old woman 10 days after
an unremarkable cesarean delivery of twins, which followed an uncomplicated pregnancy.
Diagnosis
: Delayed postpartum eclampsia with postpartum angiopathy (reversible cerebral vasoconstriction
syndrome) complicated by brain edema, ischemic, and hemorrhagic strokes.
Differential Diagnosis
:
1.
Primary Headache Disorders
: Migraine and tension-type headaches are common postpartum, but the
patient's severe and rapid-onset headaches are atypical for these types.
2.
Subarachnoid Hemorrhage
: Thunderclap headache can be a symptom, but the patient's normal brain
imaging, clear CSF, and recurrent nature make this less likely.
3.
Cerebral-Artery Dissections and Venous Sinus Thrombosis
: Thunderclap headache can occur with
these conditions, but imaging did not show evidence of cerebral venous sinus thrombosis, and the neck
arteries were not initially imaged.
4.
Postdural Puncture Headache
: Possible, but the absence of information on CSF opening pressure
makes it challenging to diagnose.
5.
Delayed Postpartum Eclampsia
: The patient's symptoms and imaging findings are consistent with
delayed postpartum eclampsia, especially given the occurrence of seizures and hypertension.
6.
Pregnancy-Related Stroke
: Risk factors and the patient's symptoms suggest pregnancy-related
stroke, but progressive multifocal vasoconstriction on MRA raises specific diagnostic considerations.
7.
Primary Angiitis of the Central Nervous System
: Unlikely due to the absence of CSF pleocytosis
and initially normal MRI and MRA.
8.
Reversible Cerebral Vasoconstriction Syndrome (Postpartum Angiopathy
): Highly suggestive due
to recurrent thunderclap headaches, benign CSF results, rapidly progressive brain edema, strokes, and
dynamic arterial changes. Treatment with calcium-channel antagonists, corticosteroids, and blood-
pressure-modulating agents is initiated.
9.
Hypertensive Small-Vessel Changes: Autopsy findings indicated mild hypertensive small-vessel
changes, which could have been a contributing factor to the patient's cerebral ischemia.
P
:
Treatment Plan
:
1.
Supportive Care
: The patient's condition rapidly deteriorated, leading to extensive cerebral infarctions
and brain edema. Supportive care, including placing an external ventricular drain was placed to monitor
intracranial pressure; the trachea was intubated, and cerebral angiography was performed while the
patient was under general anesthesia was provided in the Neuro ICU.
2.
Pharmacological Management
: The patient received various medications, including magnesium
sulfate, hydralazine, nimodipine, phenylephrine, fludrocortisone, and norepinephrine, to manage blood
pressure, cerebral perfusion, and seizures. During admission to Neuro ICU, intrathecal nicardipine,
insulin on a sliding scale, cefazolin, nafcillin, propofol (titrated to intracranial pressure) and milrinone
was started as well as intravenous phenylephrine, fludrocortisone, and intravenous norepinephrine
were administered in an effort to raise systemic blood pressure and improve cerebral perfusion.
3.
Autopsy
: An autopsy was performed to further understand the pathological changes associated with
the patient's condition.
4.
Investigation of PlGF and sFlt-1 Levels
: Blood levels of placental growth factor (PlGF) and soluble
Flt-1 (sFlt-1) were analyzed to assess their role in the pathophysiology of the patient's condition, as
they are associated with antepartum eclampsia.
5.
Alternative Treatment Options
: Pharmacologic blood-pressure modulation, calcium-channel
antagonists, and direct interventions such as balloon angioplasty or injection of vasodilators may not be
effective in preventing disease progression. Opening the artery may expose the brain to the risks of
reperfusion injury. Nevertheless, the prompt but transient relief of vasoconstriction with the use of a
vasodilator supports vasospasm as the underlying mechanism.
6.
Further Research
: Research should focus on uncovering precise mechanisms for the various
conditions included in the reversible cerebral vasoconstriction syndrome in order to develop specific
therapies.
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Case Study #2 SOAP Note
Lisa
Follow-up
: Unfortunately, despite intensive medical management, the patient's condition deteriorated rapidly,
leading to her passing away 27 days postpartum (day 8 Neuro ICU). Autopsy findings confirmed the presence
of extensive cerebral infarctions and edema. This case emphasizes the complexity and challenges in
managing severe postpartum neurological complications, particularly in the context of reversible cerebral
vasoconstriction syndrome.
Final Diagnosis
: Reversible Cerebral Vasoconstriction Syndrome (Postpartum Angiopathy).
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