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