Isolated intracranial Hydatid Cyst – Multidisplinary Approach sa •Ahmed Altibi •Heba Daradkeh •Ibrahim Nour
Isolated intracranial Hydatid Cyst – Multidisplinary Approach
sa•Ahmed Altibi•Heba Daradkeh•Ibrahim Nour
Case Presentation
saJordan University HospitalDepartment of Neurosurgery
History
A 13 year old male patient, previously healthy, living in Madaba.
Presented to our pediatrics neurology clinic on the 22nd of October, 2014.
Complaining of
HEADACHE OF ONE MONTH DURATION
History
The headache was :
- Gradual in onset.
- Initially right-sided then later became diffuse.
- Dull in nature.
He had that headache almost daily throughout the month and it was more severe upon waking up in the morning.
History
It was partially relieved with simple analgesia (Paracetamol
and Iboprufen) but did not have specific exacerbating factors.
The severity of the headache was progressively increasing,
reaching its peak a couple of days prior to his presentation.
History
The headache was sometimes associated with:
-Nausea without vomiting
-Blurring of vision
-weakness in his left upper and lower limbs, associated with numbness in the upper limb, he described difficulty carrying objects with his left upper limb. Those developed only a couple of days before his presentation.
History
NO history of :
-Fever
-Seizures
-Loss of consciousness
-trauma
-significant weight loss, poor appetite, or night sweats.
History
Past medical history: free
Past surgical history: free
No significant relevant family history
Social history:
He is the youngest in 6 brothers, lives in a rural area.
Physical Examination
General :
-In a good general condition
-Fully awake and oriented to place, time & person.
-He did look in pain !
Physical Examination
Neurological examination
-No meningeal signs
-Examination of the cranial nerves was normal
-The visual filed by confrontation test was normal
-Fundoscopic examination at the clinic showed
MILD BILATERAL PAPILLEDEMA
Physical Examination
Neurological examination ctd.
- He had an obvious left-sided PRONATOR DRIFT
- WEAKNESS in the left upper and lower limbs (4/5)
- SENSORY ATAXIA with a clear Positive Romberg’s Sign
- Deep tendon reflexes were normal
- Babinski & Hoffman’s signs were absent
Summary
a13 year old boy who presented with signs and symptoms of increased ICP :
progressive headache, postive pronator drift and mild bilateral papillaedema and
left sided weakness
Labs: CBC, Electrolytes Electrolytes were normal CBC:
Hb :12.8 WBC: 7.1 x 109
Neutrophils: 35% lymphocytes: 40% Eosinophils : 11% Basophils: 1.92% Monocytes: 5.68%
CT
MRI T1without contrast
MRI T2
MRI with contrast
Diffusion Weighted Image
Quick Summary
So this is an Intra axial supratentorial parieto-occipital cystic lesion with focal area of enhancement within its wall, no restricted diffusion, and with some vasogenic edema.
List of differentials
Is it a Pilocytic astrocytoma?
Is it an abscess?
1. Not an abscess because the DWI was free from any restricted diffusion.
These are the images of the child’s liver and lungs:
Neurosurgery
We were consulted by pediatrics teamPhysical findings were consistent with their findingsOrdered imaging were reviewed
Neurosurgery
Preparation for surgery
Patients was started on Mebendizole 3 days before the operation.
Hypertonic saline was prepared to continuously irrigate and possiblyinject the cyst if needed.
Anesthesia - Preoperative
ASA score: I
Malampati class 1
GA
ASA Standard Monitoring: Oxygenation: Pulse Oximetery Ventilation Circulation: ECG & BP Temperature
Anesthesia
Precaution Canulae (Gauge 16) Central line and arterial line
Adrenaline 50 mic Hydrocortisone Antihistamine
Imaging:
Imaging:
After surgery Transfer to ICU for observation. No postoperative complications. Complete resolution of signs
and symptoms
No Ataxia No Pronator drift No Weakness
Post OP CT
Post OP MRI with CM T2
POST OP MRI with CM
I recommend an MRI for follow up, especially that this is a child and I would want to decrease the amount of radiation he would be exposed to, also an MRI is superior in providing better characterization of the soft tissue.
Pathology
Macroscopically
Microscopically
Hydatid Disease Overview
Definition
“Hydatid Disease Is a parasitic infection by the tapeworm echinococcus.
Four species of Echinococcus produce infection in humans;
1. E. granulosus causing cystic echinococcosis (CE)
2.E. multilocularis causing alveolar echinococcosis (AE),
3. E. vogeli causing polycystic echinococcosis
4.E. oligarthrus being an extremely rare cause of human echinococcosis.
1&2 being the most common”. 8
Reproduced from: Centers for Disease Control and Prevention. DPDx: Echinococcosis. Available at:http://www.cdc.gov/dpdx/echinococcosis/index.html.
Notes on Lifecycle
Definitive host dogs or related species
Intermediate host sheep, goats, camels, horses, cattle, and swine
Humans are incidental hosts; they do not play a role in the transmission cycle. 8
Eggs are highly resistant and can remain infective for a year in a moist environment at low temperature. 8
Infectious eggs re passed to humans via fecal-oral transmission. This may occur via environmental contamination of water and cultivated vegetables or contact between infected domestic dogs and humans (often in children). 8
The same life cycle occurs with E. multilocularis (1.2 to 3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. 8
Epidemiology
Cystic hydatidosis is a significant public health problem in South America, the Middle East and eastern Mediterranean, some sub-Saharan African countries, western China, and the former Soviet Union. 8
Echinococcosis is one of the major zoonotic parasitic diseases in the Middle East and Arabic North Africa from Morocco to Egypt.
It is hyper endemic in Iran, Turkey, Iraq, Jordan, Morocco, Libya, Tunisia, and Algeria, and endemic in Egypt. 10
Both cystic and alveolar echinococcosis has been reported from these areas. However, cystic echinococcosis is more prevalent. 10
Clinical Presentation
Initially asymptomatic and may remain so for many years.
The clinical presentation depends upon the site of the cysts and their size.
Hydatid cysts may be found in almost any site of the body, either from primary inoculation or via secondary spread.
the liver (63%), lungs (25%), muscles (5%), bones (3%), kidneys (2%), brain (1%), and spleen (1%). 9
Cerebral Hydatid disease (Neurohydatidosis)
Epidemiology
Cerebral hydatid disease is a rare parasitic infestation and accounts for 1-2 % of all cystic echinococcosis. 2
“Intracranial involvement is more commonly seen in pediatric population, and 80% of patients in the recent series were children.” 7
“This high incidence in children is probably related to patent ductus arteriosus.” 7
Clinical Presentation of Neurohydatidosis
Symptoms and signs include: focal neurological deficits headaches increased intracranial pressure hydrocephalus papilledema and loss of vision altered mental status seizures (rare)
Clinical Presentation, ctd
Intracranial cysts are more frequently settled in the supratentorial compartment in the vascular territory of middle cerebral artery 1 and the parietal lobe is the most preferable site.
The other less common sites reported are skull, cavernous sinus, eyeball, pons, skull, extradural, cerebellum and ventricles.
Intracranial hydatid cysts are commonly solitary. Multiple cysts are rare. 7
Types of intracranial hydatid cysts
Primary hydatid cysts occur as direct invasion of larva that managed and filtered via liver and lung to the
brain usually solitary but may be multiple is fertile
Secondary hydatid cysts occur as a result of rupture of primary cysts in others organs then reaching by
embolization to the brain usually multiple infertile do not have brood capsule or scolices
Treatment and prognosis of neurohydatidosis
Management is surgical, with removal of the entire cyst without rupture using Dowling’s maneuver (instilling warm saline between the cyst wall and the brain) 5.
In some cases where it is felt that removing the cyst intact (without cyst rupture during surgery) is unlikely to succeed, the cyst can be removed after puncture and aspiration of its contents.
Serology and histopathology of the excised cyst will confirm the diagnosis of neurohydatidosis.
Rupture of the cyst can result in recurrence in the subarachnoid space, both intracranially and of the spine 6.
References
1. Arora SK, Aggarwal A, Datta V. Giant primary cerebral hydatid cyst: A rare cause of childhood seizure. J Pediatr Neurosci. 2014;9 (1): 73-5.
2. Polat P, Kantarci M, Alper F et-al. Hydatid disease from head to toe. Radiographics. 2003;23 (2): 475-94.
3. Senturk S, Oguz KK, Soylemezoglu F et-al. Cerebral alveolar echinoccosis mimicking primary brain tumor. AJNR Am J Neuroradiol. 2006;27 (2):
4. Binesh F, Mehrabanian M, Navabii H. Primary brain hydatosis. BMJ Case Rep. 2011;2011 (mar05 1): .
5. Ulutas M, Cinar K, Secer M. Removal of large hydatid cysts with balloon-assisted modification of Dowling's method: technical report. Acta Neurochir (Wien). 2015;157 (7): 1221-4.
6. Izci Y, Tüzün Y, Seçer HI et-al. Cerebral hydatid cysts: technique and pitfalls of surgical management. Neurosurg Focus. 2008;24 (6): E15.
7. Basarslan, S. K., Gocmez, C., Kamasak, K., & Ceviz, A. (2015). The Gigant primary cerebral hydatid cyst with no marked manifestation: a case report and review of literature. European Review for Medical and Pharmacological Sciences, 19(8), 1327–9. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/25967703
8. Pedro L Moro, MD, MPH (2016). Epidemiology and control of echinococcosis. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2016.
9. Pedro L Moro, MD, MPH (2016). Clinical manifestations and diagnosis of echinococcosis. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2016.
10. Sadjjadi, S. M. (2006). Present situation of echinococcosis in the Middle East and Arabic North Africa. Parasitology International, 55 Suppl, S197–202.