Case III Widyawan English Version

8/12/2019 Case III Widyawan English Version

1/19

0

CASE REPORT April, 2014

Wahidin Sudirohusodo Hospital

TOXOPLASMOSIS

By :

WIDYAWAN SYAHPUTRA

Supervisor : dr. cahyono kaelan, Sp.PA,Sp.S,PhD

DEPARTMENT OF NEUROLOGY

FACULTY OF MEDICINE

HASANUDDIN UNIVERSITY

2014


2/19

1

CASE REPORT

By : Widyawan Syahputra

Supervisor dr. cahyono kaelan, Sp.PA,Sp.S,PhD

I. REGISTRATIONName : Mr. F

Age : 35 year-old

Address : Bone

Registration number : 64 65 73

Admission date : January 13th

, 2014

II. ANAMNESISChief complaint: Weakness on both lower limbs

It occurred suddenly since 2 weeks before admission. The weakness was felt slowly . Starting a

sense of weight on the right leg, 3 days later spread to the left limb. Patient could still walk and did

routine activities but he felt pain on his limbs. The weakness became severe day by day until he

couldnt walk anymore. Patient worked as a farmer and often did heavy lifting. No history of backs

trauma, no history of fever, no history of hypertension, there was history of body weight loss in

recent months, there was also history of appetite loss in recent month. No history of smoking

III. PHYSICAL EXAMINATIONGeneral status: moderate illness, bad nutrition

Vital sign :

BP : 110/70 mmHg RR : 20 x/minute, thoraco abdominal

HR : 86 beats per minute, regular T : 36,8 0 C

Head : Within normal limit

Eyes : Anemic conjunctiva (-), icteric sclera (-)

Thorax : Lungs : Vesiculer, ronchi -/- wheezing -/-

Heart : Regular, sinus rhytm, no murmur

Abdomen : liver and spleen were not palpable


3/19

2

Neurological status:

GCS : E4M6V5

Higher CF : Within normal limit

Meningeal sign :Neck stiffness (-), Kernigs sign -/-

Cranial nerves : Pupils are round isocor 2,5/2,5 mm, Direct Light

Reflex +/+, Undirect Light Reflex +/+

Other cranial nerves: Within normal limit

Motoric function :

Movement N N Strength 5 5 Muscle tone N N

3 3

BPR

TPR

N N KPR

APR

PR HT

B

_ _

N N _ _

Sensoric function : Hipestesion from acral to L3 dermatom of spinal cord

Otonomic function : Urinary and alvi incontinence

IV. WORKING DIAGNOSISClinical : flaccid paraparesis

Topical : Spinal cord L3 segment

Ethiological : suspect spondylitis TB

V. TREATMENTIVFD RL : 20 drops/minute

Anti inflammation : Methyl prednisolon 125 mg /12 hours/IV

H2RA : Ranitidin 1 amp/12 hours/IV

Neurotropic : Mecobalamin 1 amp/24 hours/IM


4/19

3

VI. SUGGESTION Routine blood examination EKG AP Chest X-ray AP/Lateral lumbosacral X- ray HIV rapid test

VII. SUPPORTING EXAMINATIONLaboratory findings ( January 13

th, 2014)

Routine blood examination Blood chemistry examination

WBC : 11,94.103/mm3 Glucose ad random : 94 mg/dl

RBC : 4,94. 106/ul Ureum : 20 mg/dl

HGB : 14,0 g/dl Creatinin : 0,8 mg/dl

HCT : 39,3% Uric acid : 3,2 mg/dl

PLT : 370. 103/ul Total Cholesterol : 138 mg/dl

Trigliserida : 139 mg/dl

SGOT : 17 u/l

SGPT : 21 u/l

LDL : 183 mg/dl

HDL : 15 mg/dl

Anti HIV ( January 20th, 2014) : Non reactive

IMUNOSEROLOGI (February 10th, 2014)

IgM Anti Toxoplasma : Negatif/0,09


5/19

4

Chest X- ray ( January 13th,

, 2014 )

There are Miliar spots on both lungs field Cor with CTI within normal limit, aortic dilatation and elongation Both of sinuses and diaphragm are normal Bones are intact Impression : - Miliar TB

- Dilatatio et elongatio aortae


6/19

5

Lumbosacral X- ray (January 17th

, 2014)

o Columna vertebra lumbosacral alignment is good, no listhesiso No fraktur or bones destructiono Bones Mineralisation is goodo Intervertebralis foramen and discus are goodo Surrounding soft tissues are good

Impression : No pathological radiologic in this lumbosacral X- ray


7/19

6

Contras MRI lumbosacral ( January 22nd

, 2014)


8/19

7

o Lumbosacral vertebra is good , lordotic curve is straighto There is intrameduller spherical lesions with swelling around it as high as the level of

Th10-Th12 CV that isointens on T1WI, with ring enhancement post-contrast and

heterointens T2WI, causing central canal stenosis at these levels with dilatation of the

central canal of the scanned proximal section

o Edema of the right facet joint at the level of CV Th12-L1 and L1-L2o Edema of bilateral facet joint at the level of CV L2-L3 and CV L3-L4o Bulging disc to posterior at the level of CV L4-L5, compressed thecal sac and right

nerve root with bilateral edema of facet joint, not causing spinal canal stenosis

o Bulging disc ke posterior at the level of CV L5-S1, compressed thecal sac with bilateraledema of facet joint especially at the right side, not causing spinal canal stenosis

o Spur formation at almost all aspect level of CV lumbaliso Discus intervetebralis intensity decreases at leve of CV L4-L5 and L5-S1o Conus medullaris ends at CV L2o MR myelografi : there is no spinal canal stenosisImpression

o Intrameduller Lesion as high as CV Th10-Th12, with suggestive syringohidromyeliaof spinal ependymoma DD / astrocytoma

o Right Facet Joint edema at the level of CV Th12-L1 and L1-L2o Bilateral Facet joint edema at the level of CV L2-L3 and L3-L4o Bulging disc level CV L4-L5, compress thecal sac and right nerve root with bilateral

edema of facet joint

o Bulging disc level CV L5-S1, compressed thecal sac with bilateral edema of facetjoint especially at the right side

o Spondylosis lumbaliso Degenerative disc disease


9/19

8

Non contras head CT scan (February 4th

, 2014)

o There is isodens lesion (36.77 HU) oval shape firm boundaries with perifocal edemasurrounding it at the right parietal region which constricts the region

o Sulci and other gyri within nomal limito There is no midline shifto Other subarchnoid space and the ventricular system are within normal limito PCA, pons and cerebellum are within normal limito There is physiological calcification at pineal bodyo Paranasalis sinus and air cells mastoid are within normal limito Both orbita and retrobulber space are within normal limito Bones are intact

Impression : Mass on right parietal region susp. Astrocytoma, DD :

oligodendroglioma

Suggestion :Contrast head CT scan


10/19

9

Contras head CT scan (February 7th

, 2014)

-

o There are many round small lesions of various sizes randomly distributed on bothhemispheres, cerebellum and brain stem that enhance heterogen post-contrast especially at

the peripherial with a picture of ring enhancement and perifokal edema surrounding it,

especially in the bilateral frontotemporal

o There are also subarachnoid area enhancing post contrast in the right temporal regiono There is no midline shifto Sulci and gyri are in normal limito Ventrikel systems are within normal limito Both orbita and retrobulber space are within normal limito Paranasalis sinus and air cells mastoid are within normal limito Bones are intact

Impression : - Multiple noduls with ring enhacement suggestive infection (toxopasmosis) ?

-Meningitis appearance at right temporal region


11/19

10

VIII. FOLLOW UP

January 20th

, 2014 (8th

day of treatment)

S : The lower limbs are more difficult to move, headache

O Vital sign :


HR : 76 beats/minute , regular T : 36,8 0 C






Neurological status:

GCS : E4M6V5

Higher CF : Within normal limit

Meningeal sign :Neck stiffness (-), Kernigs sign -/-

Cranial nerves : Pupils are round isocor 2,5/2,5 mm, Direct Light

Reflex +/+, Undirect Light Reflex +/+

Other cranial nerves: Within normal limit

Motoric function :


3 2

BPR

TPR

N N KPR

APR

PR HT

B

_ _

N N _ _




12/19


13/19

12

Motoric function :


3 2

BPR

TPR

N N KPR

APR

PR HT

B

_ _

N N _ _



Therapy:

IVFD RL 20 drops/minute

H2RA : Ranitidin 1 ampul/12 hours/IV

Neurotropic : Mecoblamin 1 amp/ 24 hours/ IM

Analgetic : PDA capsul thrice a day

Benzodiazepin : Alprazolam 0,5 mg once daily at night

February 3rd

, 2014 (21st

day of treatment)

S : Headache, incoherent speech

O Vital sign :


HR : 86 beats/minute , regular T : 36,5 0 C







14/19


15/19

14

IX. DISCUSSION

A 37- year-old man was admitted to Wahidin Sudirohusodo hospital with the weakness of both

lower limbs that occurred suddenly since 2 weeks before. He felt the weakness suddenly starting sense of

weight on the right limb and 3 days later to the left limb. No history of backs trauma, no history of fever, no

history of hypertension, there was history of body weight loss in recent months, there was also history of

appetite loss in recent month and no history of smoking. Based on anamnesis and sudden weakness of both

lower limbs LMN type on physical examination, we firstly suspected this patient with flaccid paraparesis ec

spondylitis TB supporting by chest X ray (January 13 th,, 2014) that showed the imaging of miliar TB and

routine blood examination (January 13th, 2014) with a little increasing of WBC whereas other results are

within normal limit.

On January 14th, 2014 we consulted this patient to pulmonology department for the treatment of

tuberculosis, but pulmonology department refused to give anti tuberculosis drugs only from chest X ray that

mentioned miliar TB without positive BTA examination. Lumbosacral X ray result (January 17th, 2014)

showed no abnormality.Because we suspected this was an immunocompromised patient, we checked anti

HIV rapid test (January 20th, 2014) and the result was also non reactive. We kept trying to make a prompt

diagnosis. We did MRI contras lumbosacral (January 22nd, 2014) and the result showed spinal cord SOL.

Based on this result, we consulted this patient to neurosurgery department for the treatment of spinal cord

SOL and they suggested laminektomi elective operation. After several days of treatment there was no

improvement of motoric function. History of headache that occur frequently and the disturbance of higher

cortical function within last few days, neurosurgery also suggested that this patient undergo head CT scan X

ray. Expertise of non contrast head CT scan ( February 4th, 2014) showed mass of right parietal region susp.

Astrocytoma, DD: oligodendroglioma. To prove this condition, the patient underwent head CT scan

contrast examination on February 7th, 2014. The result showed the imaging of toxoplasmosis. Knowing this

condition, neurosurgery decided not to operate this patient and they didnt treat this patient anymore.They

fully trusted this patient to neurology department. To support a toxoplasmosis, we subsequently examined

blood serology anti toxoplasma on February 10th, 2014 and the result also showed negative. Without

wasting time, from the imaging of contrast CT scan, we diagnosed this patient with toxoplasmosis without

forgetting the possibility of brain tuberculoma in this patient. So we gave the toxoplasmosis therapy in this

patient combining with therapy of tuberculosis when the patient went home and he had to come back to

neurology department policlinic 3 or 4 weeks later to control his clinical improvement.


16/19

15

Toxoplasma encephalitis is an infection caused by toxoplasma gondii and involving the brain tissue.

Toxoplasma Gondi is an obligate intracellular parasite. This infections causes many clinical symptoms

varies in both humans and animals. It has a definitive host in cats. Transmission to humans can be through

direct contact with cat feces or cysts that is ingested with bad cooking food. Toxoplasma infection is most

commonly caused by reactivation of the disease that already exists prior. It generally attack patient with bad

immune system. By increasing number of HIV / AIDS, the number of encephalitis toxoplasma is also

increasing.1

Clinical symptoms of toxoplasma infection depends on the immune system of the patient. 80% of

primary cases presents asymptomatic.13The incubation period lasts about 1-2 weeks, which subsequently

either symptoms or no symptoms will progress to the chronic phase. Usually the acute phase of clinical

symptoms that present are not typical, the most common clinical symptoms are cervical lymphadenopathy,

sometimes found a slight increase in body temperature, muscle pain, pain swallowing, headache, urtica,

skin eritematous and hepatosplenomegaly so it needs a more careful examination. In symptomatic patients

these symptoms will usually disappear within a few months. Reactivation of this infection will occur when

there is a decreasing of patient's immune.2

Clinical symptoms of encephalitis toxoplasma may be impairment of mental status, persistent fever

or intermittent, headache, focal neurological deficits, anxiety until there is loss of consciousness, seizures,

vision impairment, but it can also be found meningeal sign. The occurrence of focal neurological deficits

are due to intracranial mass lesions such as hemiparesis, aphasia, cranial nerve paresis, focal seizures,

sensory deficits, sometimes also found the presence of involuntary movements, such as dystonia, chorea,

athetosis, and hemibalismus. In some patients can present with pneumonia and myocarditis. If the lesions

located in the brain stem, it will present cranial nerve disorders, disorientation, loss of consciousness and

even coma. 3

Toxoplasmosis is the most common cause of cerebral mass lesions in patients with AIDS, but appears

to be an uncommon cause of spinal cord disease. The incidence of myelopathy may be as high as 20%, with

50% of the cases reported post-mortem. Although spinal cord toxoplasmosis is uncommon, it has been

suggested that most patients with AIDS that present with evolving myelopathy, characterized by extremity

weakness, sensory involvement, absent reflexes, ataxia, incontinence, paresthesias, spinal cord enlargement,

enhancing lesions in brain or spinal cord CT or MRI, have toxoplasmic myelitis. In our patient, neurological

complaints initially present with lower limbs weakness accompanied by sensory and autonomic impairment.

But after a few days of treatment, there are other neurological deficit such as headache accompanied by a

mental status impairment.4


17/19

16

Definitive diagnosis is the detection of Toxoplasma gondii in the blood, tissues or body fluids.

Antibody examination to detect this protozoa is IgM check. Immunoglobulin (Ig) M is to detect the

presence of acute infection in the first week and IgM titers will decrease in the first week. examination of

IgM antibody using ELISA is more sensitive and shows an infection within 2-3 months. For chronic phase

IgG examination will be still visible in a few months. Suggested radiological examination is CT scan with

contrast or MRI. MRI gives better results and more sensitive than CT scan.3,5

In head CT scan without contrast, the imaging is isodens or hypodense area scattered in many places

with predilection at basal ganglia or corticomedullary junction accompanied by edema which gives mass

effect. MRI head with or without contrast can provide better imaging than CT scan. Usually these lesions

often varies from 1 cm and can be up to more than 3 cm. MRI imaging shows lesion with multiple rings,

although in some cases present with solitary lesion. Contrast MRI shows ring enhancing lesion.6,7

Diagnosis is based on clinical symptoms, risk level, the examination of IgG antibodies against

Toxoplasma gondii and supported radiological result. Besides, presumptive diagnosis can also be based on

clinical response to the treatment of toxoplasma. The closests differential diagnosis is tuberculoma,

PCNSL, tumor metastases, brain abscess. Tuberculomas are frequently encountered brain lesions in tropical

countries. Intracranial tuberculoma can occur with or without tuberculous meningitis. Numerous small

tuberculomas are common in patients with miliary pulmonary tuberculosis. 8 In our case, the imaging ofbrain contras CT scan showed numerous small enhancing lesions with history of miliar TB, so we had to

think the brain tuberculoma as the closest differential diagnosis.Therapy is given in a period of at least 6 months and divided into two parts, acute phase of treatment

that is given for about 4 to 6 weeks, followed by a maintenance phase. Corticosteroid therapy as an

adjunctive therapy to reduce brain edema, but if this toxoplasmosis occurs due to opportunistic infections, it

should be considered the giving of corticosteroid. Empirical toxoplasmosis therapy can be given to HIV

patients with CD 4 is less than 100/mm3 and obtained an imaging of brain abscess with seropositive of

toxoplasma.9,10

Acute phase therapy is started with pyrimethamine 200 mg orally followed by a dose of 75-100 mg

a day with sulfadiazine is given 1-1.5 g every 6 hours or 100 mg /kg/day (maximum dose is 8 g/day) plus

folic acid 10-20 mg/day. In patients who have an allergy to sulfa, sulfa can be replaced with clindamycin at

a dose of 600-1200 mg given every 6 hours, besides, other drugs can also be replaced as an alternative

treatment such as trimethoprim sulfametoxazole ( dose of 5 mg/kgbb/12 hours (maximum dose is 15-

20mg/kgbb/hari), azythromycin (900-1200 mg /day) orally every 12 hours. Maintenance phase therapy can

be given pyrimethamine 25-50 mg /day plus sulfadiazine 500-1000 mg/day, given 4 times a day and plus


18/19

17

folic acid. If the patient is allergic to sulfadiazine can be replaced with clydamycin 1200 mg 3 times a day.

3,11,12


19/19

Documents

Case III Widyawan English Version