Medicine Newbie: Tuberculous meningitis

Friday 6 October 2017

Tuberculous meningitis

KEYWORDS
Mycobacterium tuberculosis; antitubercular agents; case management; public health.

A. DISEASE BACKGROUND & PRESENTATION

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I. TUBERCULOSIS (TB)

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TB: Tuberculosis
BCG: Bacille Calmette-Guerrin
MDR-TB: Multidrug-resistant TB
XDR-TB: Extensively drug-resistant TB
DOT: Directly Observed Therapy

Tuberculosis (TB) is an ancient disease that is still present in many parts of the world today. It is endemic in 33 third world countries and absent in first world nations.

BCG, or bacille Calmette-Guerin, is a vaccine for tuberculosis. Many foreign-born persons have been BCG-vaccinated. BCG is used in many countries with a high prevalence of TB to prevent childhood tuberculous meningitis and miliary disease.

Malaysians must take the BCG vaccination when they first report for primary school at age 7 years. However, BCG does not provide full protection against TB. When BCG-vaccinated adults work in the hospital environment later on in life, some do acquire TB from their workplaces.

Some countries such the USA and Australia do not provide BCG vaccination as part of childhood immunization unless requested. Families who travel with unborns, newborns, babies, and young children from TB-rife countries travelling to first world nations may be safe at their destination. However, families with unborns, newborns, babies and young children from first world nations travelling to third world countries may possibly expose their family members to TB.

Today, we have an added health problem of TB coming from 3 populations - travellers and globe trotters, domestic helpers or maids, and foreign labourers. People ill with TB can infect up to 10-15 other people through close contact over the course of a year. TB is spread by airborne particles (which are moist droplets) via coughs, sneezing, speaking, singing, screaming and yelling. TB is spread through air and not by contact (touching) with the infected person.

Even though Malaysia has a good health monitoring system, TB seems to make a comeback. It was MDR-TB then, and now XDR-TB that we have to worry about now.

TYPES OF TB

There 2 types of TB, one of which is not easily detected because it is latent, and the other is obvious as it is active.

Latent TB - the bacteria remain in the body in an inactive state. There are no symptoms visible. The carrier (person) seems normal. This type of TB is not contagious. However, the TB microorganism can become active, and thus become infectious.
Active TB - the bacteria cause visible symptoms. This type of TB is infectious and can be transmitted to others.

SYMPTOMS OF TB

TB may be mild for many months before it progresses and cause more severe manifestations. Symptoms of TB include:

Chills
Fatigue
Fever
Loss of weight (LOW, weight loss)
Loss of appetite (LOA)
Night sweats

TB usually occurs in the lungs. TB of the lungs is called pulmonary TB (PTB). If TB is in the lungs (pulmonary), symptoms may include:

Coughing for longer than 3 weeks
Hemoptysis (coughing up blood)
Chest pain

EXTRA-PULMONARY TB (EPTB)

Tuberculosis can involve virtually any organ or tissue in the body. TB can occur at sites outside the lungs, and thus is referred to as extra-pulmonary TB. These sites can be bones, brain, liver, kidneys, and heart.

Bone - TB infecting the bones can lead to spinal pain and joint destruction
Brain - TB infecting the brain can cause meningitis, which manifests as tonic clonic seizures
Liver and kidneys - TB infecting the liver and kidneys can impair their waste filtration functions and lead to blood in the urine (refer Urine FEME)
Heart - TB infecting the heart (tuberculous pericarditis) can impair the heart's ability to pump blood, resulting in a condition called cardiac tamponade that can be fatal (end-points are cardiac tamponade, mortality and constrictive pericarditis).

CHEMOTHERAPY FOR EXTRAPULMONARY TB

Chemotherapy for extrapulmonary tuberculosis is initiated with INH, RIF, PZA, and EMB in an initial 2-month phase. After 2 months of 4-drug therapy, for extrapulmonary tuberculosis known or
presumed to be caused by susceptible strains, PZA and EMB may be discontinued, and INH and RIF continued during a continuation phase. Increasing evidence, including randomized controlled trials (RCTs), suggests that 6–9 month INH and RIF-containing regimens are effective for the majority of extrapulmonary sites of disease. The exception is tuberculous meningitis where the optimal duration of therapy has not been established through randomized controlled trials, but most experts and society
guidelines prescribe 12 months of treatment associated with prolonged wound discharge and scarring. Of note, the majority of lymphatic cases of mycobacterial disease in US children are caused by non tuberculous mycobacteria.

TREATMENT OF TB

Antituberculosis drugs are taken for 6 months, and there are associated risks. Non compliance (non adherence) with such a long-term antituberculosis course gives rise to MDR-TB. Follow DOT guidelines to ensure TB patients comply with taking the 6-month course of antituberculosis drugs.

The intensive phase of TB treatment consists of 4 drugs (INH, RIF, PZA, EMB):

Ethambutol (EMB)
Isoniazid (INH)
Pyrazinamide (PZA)
Rifampin (RIF)

First-line drugs

Isoniazid
Rifampin
Rifabutin
Rifapentine
Pyrazinamide
Ethambutol

Second-line drugs

Cycloserine
Ethionamide
Streptomycin
Amikacin/kanamycin
Capreomycin
Para-amino salicylic acid
Levofloxacin
Moxifloxacin

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II. TUBERCULOUS MENINGITIS

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BRAIN ANATOMY

The brain is protected by 3 layers of membrane, collectively known as meninges. The 3 membranes are the dura mater, arachnoid, and pia mater. They enclose the brain and spinal cord. Cerebrospinal fluid (CSF) fills the spaces between the membranes and cushions the brain.

MENINGITIS VS ENCEPHALITIS

Infection of the meninges by Mycobacterium tuberculosis can cause fever and seizures. Infected patients are immediately warded in the ICU and are closely monitored till they recover, if at all. Recovery is often a long process (1-2 years). Some patients may be able to recover fully, while others can only partially recover, and others die.

CHEMOTHERAPY FOR TUBERCULOUS MENINGITIS

Chemotherapy for tuberculous meningitis is initiated with INH, RIF, PZA, and EMB in an initial 2-month phase. After 2 months of 4-drug therapy, for meningitis known or presumed to be caused by susceptible strains, PZA and EMB may be discontinued, and INH and RIF continued for an additional 7–10 months, although the optimal duration of chemotherapy is not defined. Based on expert opinion, repeated lumbar punctures should be considered to monitor changes in cerebrospinal fluid cell count, glucose, and protein, especially early in the course of therapy.

In children with tuberculous meningitis, the American Academy of Pediatrics (AAP) lists an initial 4-drug regimen composed of INH, RIF, PZA, and ethionamide, if possible, or an aminoglycoside,
followed by 7–10 months of INH and RIF as the preferred regimen. There are no data from controlled trials to guide the selection of EMB vs an injectable or ethionamide as the fourth drug for tuberculosis meningitis. Most societies and experts recommend the use of either an injectable or EMB. For adults, based on expert opinion, our guideline committee prefers using EMB as the fourth drug in the regimen for tuberculous meningitis.

ADJUNCTIVE CORTICOSTEROID THERAPY

The role of adjunctive corticosteroid therapy in the treatment of tuberculous meningitis has been reported by numerous studies and an updated systematic review found a mortality benefit from the use of adjuvant corticosteroids. Therefore, we recommend adjunctive corticosteroid therapy with dexamethasone or prednisolone tapered over 6–8 weeks for patients with tuberculous meningitis.

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III. EPILEPSY

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A&E: Accident & Emergency Department

Synonyms:
Seizure(s)
Epileptic seizure(s)
Fit(s)
Electric ictus
Malay terms - tarik; nyetok; guling; rasuk; gila babi

Epilepsy may develop as a result of a brain injury, tumour, stroke, prior infection or birth defect (genetic origin).

TB infecting the brain meninges and causing meningitis is common nowadays. Patients have a characteristic fall pattern and wriggle on the floor as if struck by a lightning bolt. Some have a slight saliva output while some have a foamy mouth. The seizure may last 5 minutes or longer - and for which it becomes a medical emergency, and the patient needs to be rushed to A&E at the nearest hospital.

WHAT IS EPILEPSY?
WHAT ARE THE SYMPTOMS?

Epilepsy is a group of neurological diseases characterized by recurrent seizures.

HOW DOES SEIZURE MANIFEST?

Depending on which part of the brain is affected, a seizure may manifest as follows:

Loss of awareness
Unusual behaviours
Unusual sensations
Uncontrollable movements
Loss of consciousness

TYPES OF SEIZURES and PART OF BRAIN AFFECTED

If the abnormal electrical surge happens within a limited area of the brain, it causes PARTIAL or FOCAL seizures.
If the entire brain is involved, GENERALIZED seizures will result.

Partial seizures subdivide further to:
- Simple partial
- Complex partial

Generalized seizures subdivide further to:
- Absence seizures
- Tonic seizures
- Atonic seizures or drop attacks
- Clonic seizures
- Myoclonic seizures

MOST COMMON SEIZURE

The most common and also most dramatic are tonic-clonic seizures, also known as convulsive seizures, which are combinations of muscle stiffening and jerking. This type is what most people relate to when they think of a seizure. It also involves sudden loss of consciousness and sometimes loss of bladder control. A tonic-clonic seizure that lasts longer than 5 minutes requires immediate medical treatment.

GENERALIZED SEIZURES OF GENETIC ORIGIN

Generalized seizures that start in childhood are likely to involve genetic factors. Epilepsy due to a single gene mutation is rare. More often, an interaction of multiple genes and environmental factors is responsible. Hundreds genes have been implicated. Examples include genes encoding for GABA receptors – major components of the inhibitory circuit, and ion channels. Many genetic disorders that cause brain abnormalities or metabolic conditions have epilepsy as a primary symptom. The cause of epilepsy is unknown in about half of cases.

CAUSES OF EPILEPSY

Epilepsy may develop as a result of the following:

Brain injury (trauma or fall)
Tumour
Stroke
Previous infection
Birth defect

Babies with too much warm clothing on may suffer from seizures.
Seizures in children are caused by birth traumas, infections, congenital abnormalies, and high fevers.
Seizures in adults are caused by head injuries, infections, alcohol, stimulant drugs, side effects of medications.
Seizures in the elderly are caused by brain tumours and strokes.
Chemical causes of seizure are low blood sugar, low blood oxygen, low blood sodium, and low blood calcium.

PATHOPHYSIOLOGY OF SEIZURES

HOW DO SEIZURES HAPPEN?
WHY DO THEY HAPPEN?
PATHOPHYSIOLOGY (MECHANISM) OF EPILEPSY

NORMAL BRAIN ACTIVITY

The brain is a complex network of billions of neurons. Neurons can be excitatory or inhibitory. Excitatory neurons stimulate others to fire action potentials and transmit electrical messages, while inhibitory neurons SUPPRESS this process, preventing EXCESSIVE firing. A balance between excitation and inhibition is essential for normal brain functions.

BRAIN ACTIVITY IN EPILEPSY

Seizures happen as a result of a sudden surge in the brain’s electrical activities. In epilepsy, there is an UP-regulation of excitation and/or DOWN-regulation of inhibition, causing lots of neurons to fire SYNCHRONOUSLY at the same time.

DIAGNOSIS OF TYPE OF SEIZURE

Diagnosis is based on:

(i) Observation of symptoms
(ii) Medical history
(iii) An electroencephalogram (EEG) - to look for abnormal brain waves.
(iv) Genetic testing maybe helpful when genetic factors are suspected.

TREATMENT

There is no cure for epilepsy, but various treatments are available to control seizures.

TRADITIONAL CURE

The traditional cure used by the Malay community is freshly crushed onion. The patients lies down on a cooling pandanus mat. One big Bombay onion is coarsely pounded to yield coarsely ground juicy onion paste which is applied directly to the forehead and left to dry. A small wet towel maybe placed to avoid onion paste falling onto the eyes. The onion paste is removed when semi- or partially dry. A fresh onion paste can be re-applied if necessary, but normally one application is sufficient to cure seizure completely. This traditional method seems to work well in children whose eyeballs roll up and only the sclerae can be seen. It seems to work with children up to age 4 years, and does not recurr for 55+ years. No drugs are required when treated in this traditional manner.

TREATMENT OF EPILEPSY

The hospital provides 2 modes of treatment - dietary and drug therapies. Both are useful to control seizures. These will halt seizures and kill off M. tuberculosis.

(1) DRUG THERAPY

Medication successfully controls seizures for about 70% of cases. Many anti-epileptic drugs are available which target sodium channels, GABA receptors, and other components involved in neuronal transmission. Different medicines help with different types of seizures. Patients may need to try several drugs to find the most suitable regime for their cases.

Anticonvulsants: Phenytoin, lamotrigine

(2) DIET THERAPY

Dietary therapy: ketogenic diet has been shown to reduce or prevent seizures in many children whose seizures could not be controlled with medication. Ketogenic diet is a special high-fat, low-carbohydrate diet that must be prescribed and followed strictly. With this diet, the body uses fat as the major source of energy instead of carbohydrates. The reason why this helps control epilepsy is unclear.

Ketogenic diet reduces seizures.
Ketogenic diet is high-fat and low-carb.
When living on ketogenic diet, the body derives its energy from fat and not carbohydrates..
Ketone bodies are preferred substrates for brain energy; it utilizes ketone bodies more efficiently than glucose.
Ketone bodies are acidic as well as a cleansing agent that may cleanse the brain of unncessary firing.
The brain has a more calming effect when on ketogenic diet as occurs in strict fasting (eg Ramadan fasting).

(3) NERVE STIMULATION

Nerve stimulation therapies such as vagus nerve stimulation in which a device placed under the skin is programmed to stimulate the vagus nerve at a certain rate. The device acts as a pacemaker for the brain. The underlying mechanism is poorly understood but it has been shown to reduce seizures significantly.

(4) SURGERY

Finally, a surgery may be performed to remove part of the brain that causes seizure. This is usually done when tests show that seizures are originated from a small area that does not have any vital function.

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B. PATHOPHYSIOLOGY

Coughing 3 weeks or longer, sometimes with mucus or blood - PTB
Chills, fever & night sweats - bacterial infection
LOW, LOA & fatigue - bacterial infection
Tonic clonic seizures - meningitis

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C. DIFFERENTIAL DIAGNOSIS

Differential Diagnoses of TB:

Actinomycosis
Aspergillosis
Bronchiectasis
Constrictive Pericarditis
Fungal Pneumonia
Histoplasmosis
Lung Abscess
Nocardiosis
Non-Small Cell Lung Cancer
Pott Disease

Tuberculosis (TB) can masquerade as other infectious and disease processes, eg, congenital TB can mimic congenital syphilis or cytomegalovirus (CMV) infection.

Conditions with a presentation that may resemble pulmonary TB (PTB) (1-11) and can be included in the differential diagnosis of extrapulmonary TB include the following (1-22):

Blastomycosis
Tularemia
Actinomycosis
Mycobacterium avium-intracellulare infection
M chelonae infection
M fortuitum infection
M gordonae infection
M kansasii infection
M marinum infection
M xenopi infection
Squamous cell carcinoma
Hidradenitis suppurativa
Eosinophilic granuloma
Endemic syphilis
Erythema induratum (nodular vasculitis)
Erythema nodosum
Leishmaniasis
Leprosy
Cat scratch disease
Syphilis
Syringoma
Rheumatoid arthritis

Dermatologic differential diagnosis

Diagnosis of skin infection with M tuberculosis involves the following:

Differentiate primary-inoculation TB from ulceroglandular complexes and mycobacterioses
Differentiate TB verrucosa cutis from diseases such as North American blastomycosis, chromoblastomycosis, iododerma and bromoderma, chronic vegetative pyoderma, verruca vulgaris, verrucous carcinoma, verrucous atypical mycobacterial infection, and verrucous lupus vulgaris
Differentiate miliary TB of the skin (which appears as small, noncharacteristic, erythematous, papular or purpuric lesions) from drug reactions
Differentiate scrofuloderma from suppurative lymphadenitis with sinus-tract formation, such as blastomycosis or coccidioidomycosis
Differentiate TB cutis orificialis from glossitis, apotheosis, and deep fungal infections
Differentiate lupus vulgaris from lupoid rosacea, deep fungal or atypical mycobacterial infection, chronic granulomatous disease, granulomatous rosacea, and Wegener granulomatosis
Differentiate erythema induratum from nodular panniculitides (eg, Weber-Christian disease) and nodular vasculitides (eg, syphilitic gumma, nodular pernio)
Differentiate papulonecrotic tuberculid from other papulonecrotic entities, such as leukocytoclastic vasculitis, lymphomatoid papulosis, papular eczema, and prurigo simplex with neurotic excoriation
Differentiate lichen scrofulosorum from keratosis spinulosa, lichenoid sarcoid, and lichenoid secondary syphilis

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D. INVESTIGATIONS

TB is diagnosed by skin tests, blood tests, x-rays, and other tests.

Radiology - Chest radiograph; Brain and spine imaging - Imaging techniques: X-ray, CT-scan, MRI. Monitoring brain activity pattern: EEG. An EEG may also help in differentiating between partial and generalized seizures. EEG and MRI/CT-scan are tools to monitor the brain in unconscious patients.
Chemical Pathology - CSF Biochemistry - CSF protein (increased due to active infection), CSF glucose (reduced due to active infection); Renal function tests (RFT)
Microbiology - Tuberculin skin test; sputum test; Gram stain (Gram-); Ziehl-Neelsen stain for AFB; C&S - susceptibility and dose; Molecular techniques - DOT immunobinding assay for TB Ab
Hematology - Coagulation profile
Pathology - Autopsy: if brain death occurs
Genome - Genetic studies: Causes of lowered immunity - HIV/AIDS, coinfection (PCR)
Community Medicine - social and community studies; carrier status of family members
Ophthalmology - Visual acuity and red-green color perception testing

(1) RADIOLOGY

Imaging techniques are X-ray, CT-scan, and MRI.

Chest radiograph
Brain and spine imaging

(2) MEDICINE, ANAESTHESIOLOGY & ANATOMY

SPINAL TAP

A spinal tap is performed to obtain CSF. The spinal tap is of 3 types, each puncture giving different characteristics for the CSF harvested. Lumbar puncture is the usual one performed to obtain CSF. There are risks associated with spinal tap.

Lumbar puncture
Cisternal puncture
Ventricular puncture

At HUSM, the CSF is collected into a sterile 20-ml vial with a yellow screw cap and sent for CSF Biochemistry.

(3) CHEMICAL PATHOLOGY

In the Chemical Pathology laboratory, a CSF specimen may show up as often as once every 2 days (ie about 10 CSF specimens per month). These samples can come from both pediatric as well as adults patients.

CSF and serum are analysed for various analytes. For CSF Biochemistry, there are 2 major analytes that are measured - ie CSF protein and CSF glucose. These tests are done on an automated chemistry analyser. CSF protein is elevated in tuberculous meningitis while CSF glucose is reduced.

Serum samples are obtained from blood specimens and are analysed for Renal Function Tests (RFT) and Liver Function Tests (LFT). All these chemistries are categorised as STAT and their analyses are performed ASAP. They are performed on automated chemistry analysers and the turnaround time (TAT) for these tests are less than an hour.

Patients with TB who are receiving pyrazinamide (PZA) should undergo baseline and periodic serum uric acid assessments.

CSF >> For CSF Biochemistry >> CSF protein & CSF glucose. Other analytes are included as required.
BLOOD >> SERUM >> Renal Function Tests (RFT) are performed to detect kidney involvement if any. RFT includes Sodium, Potassium, Chloride, and Creatinine.
BLOOD >> SERUM >> Liver Function Tests (LFT). LFT is performed to detect liver involvement, if any. LFT includes AST, ALT, Bilirubin, and ALP. Other causes of abnormal LFT should be excluded, if any (see HIV).*
BLOOD >> SERUM >> Uric acid.

(4) MICROBIOLOGY

PPD: purified protein derivative
IGRA: interferon-gamma release assay
DNA: deoxyribonucleic acid
rRNA: ribosomal RNA
PCR: polymerase chain reaction
PCR-RFLP: polymerase chain reaction-restriction fragment length polymorphism
NAAT: Nucleic Acid Amplification Tests
MODS: Microscopic-observation drug susceptibility (MODS) assay
TLA: thin-layer agar (TLA) assay

For Microbiology tests, CSF, sputum and bacterial isolates are tested when available. Sputum is the main specimen for PTB. Sputum is used for Culture and TB Drug Susceptibility Testing. However, in extra-PTB, and when there is no sputum, and other means of testing are tried.

Since conventional Microbiology techniques are time-consuming (3 weeks to 1 month), more recent/newer test methodologies are constantly being developed. These deploy molecular techniques (eg PCR, PCR-RFLP) and use either DNA or rRNA of the mycobacterium as samples. Some of these new/recent tests which have been developed are NAAT, MODS and TLA assays. These assays are less time-consuming and turnaround time (TAT) for results are shorter (about 2 weeks).

For CSF Microbiology, detection of the mycobacterium is done by the Microbiology lab and involves the following tests:

Skin on left forearm >> Mantoux tuberculin skin test using PPD. For detecting latent TB and previous exposure to TB or BCG. Noticeable bump (induration) larger than 5 mm/10 mm/ 15 mm diameter are positive Mantoux. The diameter is marked with a ballpoint pen as 2 black dots and the distance between the 2 dots is measured in mm.

An itchy red bump measuring 15mm indicates a positive Mantoux test.
The ballpoint pen outline is the size of a 50 sen coin.

Blood >> Serum >> An in vitro blood test based on IGRA with antigens specific for M tuberculosis can also be used to screen for latent TB infection and offers certain advantages over tuberculin skin testing.
Sputum >> Mycobacterial culture and sensitivity (C&S) is done to plate out and isolate M. tuberculosis. MTB is isolated and identified. Its susceptibility to INH, RIF, PZA, EMB is determined.
Sputum >> An automated molecular test that uses sputum samples for the detection of M tuberculosis and resistance to rifampin has been developed.
Sputum >> Gram stain: Gram negative (Gram- pink rods)
Sputum >> Culture for acid-fast bacilli (AFB) and smear microscopy. M. tuberculosis is spread on a microscope slide and stained with Ziehl-Neelsen stain. M. tuberculosis are Gram- rods which appear as bright pink bullets under the microscope.
Sputum >> TB Drug susceptibility testing. DNA sequencing analysis (PCR-RFLP) is a rapid and useful method for detecting drug-resistant TB.
Bacterial isolate >> Nucleic Acid Amplification Tests (NAAT): DNA probes specific for mycobacterial rRNA identify species of clinically significant isolates after recovery. In tissue, PCR amplification techniques can be used to detect M tuberculosis-specific DNA sequences and thus, small numbers of mycobacteria in clinical specimens.
Sputum >> TB Drug susceptibility testing >> Microscopic-observation drug susceptibility (MODS) and thin-layer agar (TLA) assays are inexpensive, rapid alternatives to conventional and molecular methods of TB drug susceptibility testing.
Blood >> Serum >> Hepatitis B and C screen

*Culture-Negative Pulmonary Tuberculosis in Adults
Failure to isolate M. tuberculosis from appropriately collected sputum specimens in persons who, because of clinical or radiographic findings, are suspected of having pulmonary tuberculosis (PTB) does not exclude a diagnosis of active tuberculosis. Some causes of failure to isolate organisms include low bacillary populations, inadequate sputum specimens, temporal variations in the number of expelled bacilli, overgrowth of cultures with other microorganisms, and errors in specimen processing

(5) IMMUNOLOGY

IRIS: immune reconstitution inflammatory syndrome
ART: antiretroviral therapy

HIV serology testing

*HIV/AIDS

Patients with HIV infection and tuberculosis are at increased risk of developing paradoxical worsening of symptoms, signs, or clinical manifestations of tuberculosis after beginning antituberculosis and antiretroviral treatments.
These reactions presumably develop as a consequence of reconstitution of immune responsiveness brought about by ART, and are designated as the immune reconstitution inflammatory syndrome (IRIS).
Tuberculosis IRIS has been noted to be more common in participants with earlier ART initiation and CD4+ cell counts less than 50 cells per microlitre.
Signs of IRIS may include high fevers, worsening respiratory symptoms, increase in size and inflammation of involved lymph nodes, new lymphadenopathy, expanding central nervous system lesions, worsening of pulmonary parenchymal infiltrations, new or increasing pleural effusions, and development of intra-abdominal or retroperitoneal abscesses .

(6) HEMATOLOGY

Anticoagulants: Warfarin

Monitoring blood coagulation is necessary.

Prothrombin time (PTT)
Platelet count
Complete blood cell (CBC) count

*(7) PATHOLOGY & PHARMACOLOGY

Viral hepatitis (hepatitis A, B, and C in all patients; Epstein-Barr virus, cytomegalovirus, and herpes simplex in immunosuppressed patients)
Biliary tract disease
Other hepatotoxic drugs (eg, acetaminophen, acetaminophen-containing multiagent preparations, lipid-lowering agents, other drugs)
Select herbal and dietary supplements

(8) SOCIAL/COMMUNITY MEDICINE and PSYCHOLOGY

Weight
Vision assessment
Diabetes screen
Alcohol
HIV/AIDS

Psychotropic drugs

Nortriptyline
Haloperidol, quetiapine
Benzodiazepines (eg diazepam, triazolam), zolpiderm, buspirone

(9) OPHTHALMOLOGY

Patients with TB who are receiving long-term ethambutol (EMB) therapy should undergo baseline and periodic visual acuity and red-green color perception testing. The latter can be performed with a standard test, such as the Ishihara test for color blindness.

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E. DIAGNOSIS

A positive TB skin test or TB blood test only tells that a person has been infected with TB bacteria. It does not tell whether the person has latent TB infection (LTBI) or has progressed to TB disease. Other tests, such as a chest x-ray (CXR) and a sample of sputum, are needed to see whether the person has TB disease.

Tuberculous meningitis (TBM)

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F. TREATMENT AND MANAGEMENT

Refer to sections above on Treatment for TB and Treatment for Seizures.

Isolation of TB patients (wards and ICU) are necessary to avoid further transmission
In patients with tuberculous meningitis, dexamethasone added to routine 4-drug therapy reduces complications.
DOT is necessary to ensure patients take their medications for 6 or 9 months
Monitoring the desired and adverse effects of the drugs is necessary

Monitoring

Patients diagnosed with active TB should undergo sputum analysis for Mycobacterium tuberculosis weekly until sputum conversion is documented. Monitoring for toxicity includes baseline and periodic liver enzymes (AST, ALT, ALP), complete blood cell (CBC) count, and serum creatinine.

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G. MERCI

Medical (M)
An epileptic patient needs help when unconscioous or sub-conscious or when falling.
Falling and hitting the head may cause further injury to the H&N region.

Empathy (E)
An epileptic patient needs comforting, help and care during a seizure and post-seizure.

Rights and Respect (R)
Epileptic patients have the same rights and must be respected just like you and me.

Communication (C)
Talking to the patient pre- and post-seizure must be gentle and soothing so as not to create depression (blues) and more harm.
There are instances when epileptic patient must not drive. Seeing to patient compliance is very important.

Insight (I)
Timing and recording the characteristics of each seizure are important.
The duration between seizures is important to know.
Keeping a close watch on epileptic patient is important.
Seeing to that epileptic patient takes his/her medicine is important.

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External links:

TB
https://www.medicalnewstoday.com/articles/8856.php
https://medlineplus.gov/tuberculosis.html

Friday 6 October 2017

Tuberculous meningitis

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