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Interesting Case RoundsNadim J Lalani
20.07.2006
Patient C.B : 53 y.o. ♀ Transferred to FMC CCU from Red Deer with
Acute MI PMHx:
HTN Depression Etoh Abuse COPD on home O2 VP shunt 1996 [Obtructive Hydrocephalus due to
benign mass] shunt revision ‘98
Pt C.B. Meds:
Avalide Wellbutrin Imipramine Effexor Tryptophan
Smoker has many cats
HPI: March 17 experiencing chest pain and HA
Agitated, was pacing & collapsed EMS to Innisfail Hospital
In ED: Vitals: 369, hr 119, 35, 106/80, Some respiratory distress. Neuro: “Confused but following commands”
R pupil 5mm > L 4mm plantar response: ↑ ↑
Agitated
Innisfail ED [cont’d]:
Given:
Asthma cocktail
Ativan for agitation
Transferred to Red Deer:
Confusion / agitation / sob
Red Deer Hospital: Confused,agitated,restless, intermittent
fevers Vitals: Afeb 120, 24, 100/75,93%
Altered LOC, GCS 6,pupils variable
? ↑ tone, rambling speech
Red Deer Hospital [cont’d] Initial Labs:
ABG: 7.37/41/116/24
Hb 137, WBC 15.2, Plt 264
CK 559 (< 140 u/L)
Acetominophen/ ETOH/ ASA: all NEG
CXR: Hyperinflation EKG: N Admitted with the following issues:
COPD
? Seratonin Syndrome
? Etoh Withdrawal
Red Deer Hospital [Cont’d] Next 24 - 48H:
Improved on IV fluids, multi-vits
Solu-medrol & withholding psyc
meds. March 20: breathlessness, ↓ LOC
CXR: mild oedema
ABG: 7.35/72/135/40
Intubated
had following EKG:
Red Deer Hospital [cont’d] Next 24H: extubated, more alert & lucid
EKG: T-wave changes Echo: akinetic apex TNi 7.11 (0-0.10ug/L) (>1.5
ug/L= MI) CK 1751
CT head: Reported as Normal
Pt transferred to FMC Cardiology Dx: MI on Nitro drip and Heparin
En route to Foothills Hospital: Patient:
became lethargic, gasping
GCS decreased to 8
pupils unequal
intubated (again)
Foothills Hospital CCU [Mar 22]: Exam:
VSS
Intubated, withdrawing,
opens eyes to pain
reflexes 4+ LE’s
? ↑↑ tone , 4 beat clonus
shunt depresses and fills
completely
What’s going on?
CCU: Gets Repeat CT
March 22 [cont’d] NeuroSurgery Consulted ? Shunt Malfxn Initial exam:
Intub, withdrawing
disconjugate gaze
Drain off 20cc via shunt reservoir Pt immediately awakes, begins reaching for ETT Cannot palpate distal shunt got AXR:
March 23-26: Further 20 cc drained off [02:00 am] In a.m Cardiac cath: Normal Coronaries Echo: Mild LV hypokinesis Pt had shunt studies went to OR third ventriculostomy Pt does well. Discharged home
HydroCephalus First described by Hippocrates Epidemiology: 1.2/1000 live births Disturbance of CSF flow
CSF physiology Secreted by Choroid
Plexus [20ml/h] Passive absorption:
SA space venous system
Mostly obstruction [except choroid papilloma]
Causes of Hydrocephalus
Prematurity (posthemorrhagic)
Myelomeningocoele
Other congenital (Aqueductal stenosis &c.)
Brain tumor
Subarachnoid hemorrhage
Meningitis
Shunts Three Parts:
Ventricular catheter Valve Distal Catheter
Diverted to: Peritoneum Pleural Cavity GB, RA, IJ
Lumbar CSF Shunts
Shunts
Shunt Malfunction Two categories :
Shunt Failure Infection
Infection : Coag negative Staph Fevers/malaise meningitis Important to r/o in paeds presentation
Shunt Failure Shunt Failure:
Debris Component failure Fracture/ separation/ migration
30-40% fail within 1st year 15% failure in 2nd year After 2nd year 1-5% failure /year Mortality 1-4%
Assessment Hx: [ incr ICP]
HA [morning], neck pain N/V Irritability, gait problems, recent VP shunt
P/E: Papiloedema CN VI palsy ,CN III palsy “Sunsetting” ALOC / Coma Don’t forget to palpate the shunt
Hx & P/E not very sensitiveSens Spec
Nausea /Vomit36 97
HA 15 97ALOC 10 100Papilloedema 3 100
Usefulness of balloting the shunt? Rationale:
If it depresses patent distally If it refills patent proximally
Reality: Sensitivity only 20% in the hands of Nsx! Even “positive” test not useful [25% false]
Radiography? Shunt Survey [XR skull, Chest , KUB]:
Sensitivity 20% LR –ve 0.82
CT: 83% sens LR –ve 0.21
Combined : 88 sens BUT!
1 in 8 pts with obstruction have normal studies
Diagnostics Shunt study:
Test of choice Usually NSx has to order
Tapping the shunt: Easy to do / therapeutic Can send CSF [Can measure ICP]
Tapping the Shunt Sterile Prep 25 gge Butterfly Tubing/syringe Take off 20 cc at a
time
What about the “MI” ?:
Neuro-mediated Cardiac Stress: Electrocardiographic abnormalities well described
for SAH TWi, ST ↑ Long QT &c. Originally thought to be
benign SAH now known to cause:
significant increases in ICP, Increased cardiac outputSignificant changes in creatine kinase and catecholamines
Furthermore, Pts with SAH and ST ↑have been shown to have impaired contractility “neurogenic stunned myocardium”
One other Report of this related to hydrocephalus from choroid cyst
But now recognise that both psychiatric physiologic stressors can cause an “MI” picture.
Transient LV dysfunction Clinically resembles acute myocardial infarction
Characteristics of:
transient/reversible LV dysfunction with chest painEKG changesrelease of cardiac enzymes hypokinesis of LV on echo Normal coronary arteries
Clinically: elderly women over 60 years of age some physical or mental stress precedes
the onset of the symptom Most common presenting symptom is chest
pain or dyspnea Often CHF from decreased left ventricular
systolic function
Diagnostics: EKG findings classically initial ST elevation ST depression Deep symetric T wave inversion Abnormal QT Small or moderate elevation of cardiac
enzymes (large elevations unusual)
Etiology/Associated Events: Emotional stress (death of loved one, panic
d/o) Pneumothorax, resp distress, subarachnoid haemorrhage Trauma Phaeochromocytoma Guillain-Barré syndrome
Pathophysiology: Animal/perfusion models support idea that
it is likely the result of catecholamine surge involves microvascular perfusion AbN In some it involves coronary artery spasm
Pt C.B: Psych Hx Female, Over 50 Chest pain and dyspnea Echo that had apical hypokinesis ST↑ that progressed to deep TWi and ↑QT Normal Cath
Voila!
Questions?
References:1.Physical examination of Patients With cerebrospinal Fluid Shunts: Is There Useful Information in
Pumping the Shunt? Joseph H. Piatt
Pediatrics 1992; 89(3):470-473.
2. Pitfalls in the diagnosis of ventricular shunt dysfunction: radiology reports and ventricular size.
Iskandar BJ, McLaughlin C, Mapstone TB, Grabb PA Oakes WJ Pediatrics 1998; 101 (6): 1031-6
3. Evaluation of Hydrocephalus Shunts in the Emergency Room
Robert C Dauser
Emergency Medicine Clinics of North America 1987; 5 (4): 709-717
References :4.Radiographic evaluation for suspected cerebrospinal fluid shunt obstruction.
Zorc JJ, Krugman SD, Ogborn J, Benson J. Pediatr Emerg Care. 2002 Oct;18(5):337-40
5.Ventriculoperitoneal shunt block: what are the best predictive clinical indicators?
Barnes NP, Jones SJ, Hayward RD, Harkness WJ, Thompson D.
Arch Dis Child. 2002 Sep;87(3):198-201.
6. Akashi et al. The clinical features of takotsubo cardiomyopathy. Q J Med. 2003: 96:563-573
7.Characterization of the cardiac effects of acute subarachnoid hemorrhage in dogs.
Elrifai AM, Bailes JE, Shih SR, Dianzumba S, Brillman J.Stroke. 1996 Apr;27(4):737-41
8.Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium.
Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. J Am Coll Cardiol. 1994 Sep;24(3):636-40.
9.Myocardial injury and left ventricular performance after subarachnoid hemorrhage.
Mayer SA, Lin J, Homma S, Solomon RA, Lennihan L, Sherman D, Fink ME, Beckford A, Klebanoff LM. Stroke. 1999 Apr;30(4):780-6.
Roberts: Clinical Procedures in Emergency Medicine, 4th ed., Copyright © 2004
Garton HJL and Piatt JH Hydrocephalus.Pediatr Clin N Am 51 (2004) 305-325