ICU Case Presentation VSR 3 20051013 Name xx

  • Slides: 68
Download presentation
ICU Case Presentation VS洪國華大夫/R 3 邱威儒 2005/10/13

ICU Case Presentation VS洪國華大夫/R 3 邱威儒 2005/10/13

Name: 金xx n Gender: Male n Age: 35 (59/10/22) n Date of admission: 94/08/15

Name: 金xx n Gender: Male n Age: 35 (59/10/22) n Date of admission: 94/08/15 n

Chief Complaint n Dizziness and spinning sensation since 1 month ago before this admission

Chief Complaint n Dizziness and spinning sensation since 1 month ago before this admission

Present Illness (1) n This 35 years old patient had been in usual health

Present Illness (1) n This 35 years old patient had been in usual health before. He was a criminal. According to his statement, he suffered from dizziness and spinning sensation for 30 minutes, 3 -4 times in that month just before admission

Present Illness (2) He also had the symptoms of lowpitch tinnitus of bilateral ears,

Present Illness (2) He also had the symptoms of lowpitch tinnitus of bilateral ears, hyperacusis and vertigo that was not posture-related. n Besides, chest tightness, palpitation, SOB, hand numbness, and tremor were also complained. n

Present Illness (3) n He was brought to 署東 hospital, according the medical transferal

Present Illness (3) n He was brought to 署東 hospital, according the medical transferal sheet, his brain CT on 94/08/04 had no abnormal finding, PES showed mild GU, abdominal echo showed fatty liver and biochemistry showed no abnormal datum.

Present Illness (4) n n He was brought to our ER on 94/08/07. Mild

Present Illness (4) n n He was brought to our ER on 94/08/07. Mild leukocytosis (WBC was 10600/u. L) with neutrophil predominant (85. 2%) was noted. Hypokalemia and hyponatremia were also noted(Na was 132 meq/L and K was 3. 3 meq/L) He was arranged neurologic OPD follow up on 94/08/08. Peripheral vertigo was suspected.

Present Illness (5) He was brought to our ER again due to progressed symptom

Present Illness (5) He was brought to our ER again due to progressed symptom and blurred vision of right eye. Hearing impairment was noted, especially right ear. n Brain CT was done at ER n

Present Illness (6) Brain CR on 94/08/14 n 1. 2. 3. 4. 5. 6.

Present Illness (6) Brain CR on 94/08/14 n 1. 2. 3. 4. 5. 6. 7. 8. 9. n IMP: Not conclusive for lesion n n n n No soft tissues swelling in skull vault Normal contour quadrigeminal and basal cisterns Ventricles appropiate for age Symetry of skull Normal calcifications in pineal body Paraventricle white matter and cortex unremarkable Basal ganglia and internal capsule intact Brainstem & cerebellum unremarkable No abnormality in bone window, eyeball

Lab data at ER n n n n Hb 14. 8 gm/d. L HT

Lab data at ER n n n n Hb 14. 8 gm/d. L HT 42. 7% WBC 15500/ul Seg 87. 4% Eosi 0. 1% Baso 0. 4% Mono 3. 9% Lym 8. 2% Glucose(AC) Creatinine K Na 220 MG/DL 0. 8 MG/DL 2. 4 MEQ/L 128 MEQ/L 【URINE】 SCREEN TEST Specific Gravity 1. 020 p. H 7. 5 Protein Glucose Trace Ketone Bodies Bilirubin Occult Blood Urobilinogen 1. 0 EU/DL Leukocyte Nitrite SEDIMENTS RBC 0 -2 /HPF WBC 0 -2 /HPF Epithelium cell 0 -2 /HPF Amorphous phosphate 2+ Bacteria 2+

ER course Consult Ophthalmologist: disc edema, ou n Admission under the impression of electrolyte

ER course Consult Ophthalmologist: disc edema, ou n Admission under the impression of electrolyte imbalance (Hypokalemia, hyponatremia), leukocytosis, r/o sepsis, vertigo and visual blurred vision of right eye suspected disc edema related. n

Past Medical History n n n Allergy: Denied Childhood diseases: Denied Know illness ,

Past Medical History n n n Allergy: Denied Childhood diseases: Denied Know illness , Operation, Hospitalization: in usual health before

Personal Health Habits & Family history Diet: poor appetite n Tobacco: unknown n Alcohol:

Personal Health Habits & Family history Diet: poor appetite n Tobacco: unknown n Alcohol: denied n Betel: denied n Current Medication: Erispan, Cedol, Ativan as OPD drug n Family history: mother had brain abscess at NTH, OP by NS n

Physical Examination(1) • • • Status on Arrival: clear, E 4 M 6 V

Physical Examination(1) • • • Status on Arrival: clear, E 4 M 6 V 5 Height: 165 cm Weight: 54 kg Vital Signs: BP: 180/100 mm. Hg BT: 37℃ PR: 76/min RR: 18/min n HEENT: with normal limit CHEST: symmetrical expansion, breathing sound: few bilateral basal, no wheezing HEART: Regular heart rhythm, No Murmur n n

Physical Eximination(2) ABDOMEN: Soft and flat, no tenderness n EXTREMITIES & SPINE: Free and

Physical Eximination(2) ABDOMEN: Soft and flat, no tenderness n EXTREMITIES & SPINE: Free and movable, no pitting edema n SKIN: Normal skin turgor, no abnormal skin lesion n Neurogical: Right side blurred vision and hearing impairment. No obvious neck stiffness n

Impression 1. Electrolyte imbalance(Hypokalemia, hyponatremia) n 2. Leukocytosis, r/o sepsis n 3. Vertigo and

Impression 1. Electrolyte imbalance(Hypokalemia, hyponatremia) n 2. Leukocytosis, r/o sepsis n 3. Vertigo and visual blurred vision of right eye, cause to be determined n 4. Disc edema, OU, r/o CNS infection or brain lesion? n

Hospital day 1 - 94/08/16 Lab Data n n n n n Glucose(AC) Protein

Hospital day 1 - 94/08/16 Lab Data n n n n n Glucose(AC) Protein Albumin A/G Ratio Direct Bilirubin Total Bilirubin ALK-Phosphatase AST(GOT) ALT(GPT) Total Cholesterol Triglyceride BUN Uric Acid Creatinine K Na Cl P Osmolarity 117 mg/d. L 6. 7 GM/DL 3. 6 g/d. L 1. 2 0. 2 mg/d. L 0. 7 mg/d. L 65 IU/L 21 IU/L 31 IU/L 167 mg/d. L 48 mg/d. L 2. 9 mg/d. L 0. 7 mg/d. L 2. 4 m. Eq/L 127 m. Eq/L 90 m. Eq/L 2. 0 mg/d. L 272 MOS/KG Hb 14. 3 gm/d. L RBC 4. 63 10^6/u. L HT 41. 6 % MCV 89. 8 uu WBC 16600/u. L WBC-DC Neut 89. 0% Eosin 0. 0% Baso 0. 0% Monocyte 5. 0 % Lymphocyte 6. 0 % CRP 2 mg/DL 【URINE】 K 19. 4 MEQ/L Na 29 MEQ/L Cl 42 MEQ/L P 29. 6 MG/DL Ca 12. 1 MG/DL Creatinine 49. 6 MG/DL Mg 4. 0 MEQ/DAY Osmolality 337 MOS/KG TTKG = 6. 5

Hospital day 1 94/08/16 Neurologist consultation-Imp: • r/o CNS infection with IICP (Herpes simplex

Hospital day 1 94/08/16 Neurologist consultation-Imp: • r/o CNS infection with IICP (Herpes simplex encephalitis should be ruled out) • r/o Autoimmune disease

Hospital day 2 94/08/17 n n n Lumbar puncture-Open pressure 220 mm. H 2

Hospital day 2 94/08/17 n n n Lumbar puncture-Open pressure 220 mm. H 2 O; Close pressure 175 mm. H 2 O 【CSF】 Glucose 63 MG/DL Protein 52 MG/DL Cl 111 MEQ/L LDH 16 U/L n n n n n Color Watery Appearance Clear Pandy's Test Positive RBC 45/CMM WBC 378/CMM L: N M 7 L 92 N 1 E 0

Hospital day 2 94/08/17 Conscious: delirium n Rocephin and Acyclovir were prescribed empirically for

Hospital day 2 94/08/17 Conscious: delirium n Rocephin and Acyclovir were prescribed empirically for CNS infection n KCl supply n Glycerol for IICP n

Hospital day 3 94/08/18 n n n n 【CSF】 S. Penumonia Ag(CSF) H. Influenza

Hospital day 3 94/08/18 n n n n 【CSF】 S. Penumonia Ag(CSF) H. Influenza Ag(CSF) N. Meningitis Ag(CSF) β-Strep. group B(CSF) Cryptococcus(CSF) India Ink stain-CSF n n Cryptococcus neoformmans were seen. AFB stain-CSF n Negative 2048 x + No AFB were seen.

n n n TSH FREE T 4 Cortisol 0. 13 u. IU/ml 0. 35

n n n TSH FREE T 4 Cortisol 0. 13 u. IU/ml 0. 35 - 5. 50 1. 62 ng/dl 0. 89 - 1. 76 33. 80 MG/DL AM 4. 3 -22. 4 PM 3. 09 -16. 66 ACTH 61. 30 pg/ml 0. 00 - 46. 00 Plasma Renin Activity 0. 8 pg/ml 立: 1. 5 -5. 7 臥: 0. 2 -2. 8 EEG: indicative of diffuse cortical dysfunction such as encephalitis

Hospital day 3 94/08/18 DC Acyclovir, DC Rocephin n. Diflucan(100) 6 vial qd n

Hospital day 3 94/08/18 DC Acyclovir, DC Rocephin n. Diflucan(100) 6 vial qd n Cardiopulmonary arrest on 6: 06 pm n. CPCR for 25 mins n. Regained vital sign but bilateral pupil dilatation and no light reflex n

Hospital day 3 94/08/18—Lab data during CPR n n n n n Hb 16.

Hospital day 3 94/08/18—Lab data during CPR n n n n n Hb 16. 0 gm/d. L HT 47. 1 % WBC 12300 /ul WBC-DC Seg 88. 6 % Eosin 0. 0 % Baso 0. 2 % Monocyte 3. 6 % Lymphocyte 7. 6 % PLATELET 329000 /ul PT Patient 13. 2 sec. Control 11. 7 sec. INR 1. 25 INR APTT Patient 26. 3 sec. Control 30. 6 sec. n n n n Glucose(AC) BUN Creatinine K Na Cl AST(GOT) Ammonia Amylase CK CKMB Troponin-I D-Dimer 232 MG/DL 10 MG/DL 1. 1 MG/DL 3. 3 MEQ/L 133 MEQ/L 112 MEQ/L 26 U/L 16 ug/dl 61 U/L 730 U/L 13. 2 U/L 0. 34 ng/ml >=4. 0<8. 0 ug/ml

Hospital day 3 94/08/18—EKG post CPR

Hospital day 3 94/08/18—EKG post CPR

Hospital day 3 -94/08/18 Switch Diflucan to Amphotericin B n Shock status under inotropics

Hospital day 3 -94/08/18 Switch Diflucan to Amphotericin B n Shock status under inotropics n Polyuira, urine SG 1. 000, suspected central DI n n IVF supply and DDAVP 2 puff q 6 h

Hospital day 4 94/08/19 n n n n 【URINE】 Glucose 4 MG/DL K 10.

Hospital day 4 94/08/19 n n n n 【URINE】 Glucose 4 MG/DL K 10. 1 MEQ/L Na 44 MEQ/L Cl 53 MEQ/L Creatinine 12. 3 MG/DL Osmolality 161 MOS/KG DDAVP(4 mcg) 4 amps n n n n 【URINE】 Glucose 2 MG/DL K 8. 0 MEQ/L Na 116 MEQ/L Cl 126 MEQ/L Creatinine <10. 0 MG/DL Osmolality 280 MOS/KG

Hospital day 4 -94/08/19 n HCV Ab Negative 0. 43 S/CO HBs. Ag Negative

Hospital day 4 -94/08/19 n HCV Ab Negative 0. 43 S/CO HBs. Ag Negative 0. 7 S/CO C 3 137 MG/DL C 4 29 MG/DL RA <20. 0 IU/ML Antinuclear Factor Negative HIV Ab= 0. 00 (Negative) n Patient AAD on 13: 15 PM n n n

Fungus Culture-Blood: No Growth in 6 Weeks. n Roultine Culture-Blood: No Growth in 5

Fungus Culture-Blood: No Growth in 6 Weeks. n Roultine Culture-Blood: No Growth in 5 days for 2 sets n CSF fungus culture: Cyrptococcus neoformans. Fluconazole MIC: 12 ug/m. L n

Final Diagnosis 1. 2. 3. 4. 5. Cryptococcus neoformans meningitis Septic shock with cardiac

Final Diagnosis 1. 2. 3. 4. 5. Cryptococcus neoformans meningitis Septic shock with cardiac arrest post CPR Polyuria (central diabetes insipidus + reactive hyperglycemia+ Saline hydration related) Electrolyte disorder (hypokalemia, hyponatremia, hypernatremia) Abnormal liver function test

Discussion Cryptococcal Meningitis

Discussion Cryptococcal Meningitis

n n Cryptococcus neoformans is an encapsulated yeast. Virulence probably plays a relatively small

n n Cryptococcus neoformans is an encapsulated yeast. Virulence probably plays a relatively small role in determining the outcome of an infection. The crucial factor is the immune status of the host. defective cell-mediated immunity. n AIDS, organ transplantation, reticuloendothelial malignancy, corticosteroid treatment (but not those with neutropenia or immunoglobulin deficiency), sarcoidosis

Mycology n n C neoformans has 2 varieties— neoformans and gattii. The species has

Mycology n n C neoformans has 2 varieties— neoformans and gattii. The species has 4 serotypes based on antigenic specificity of the capsular polysaccharide; serotypes A and D (C neoformans var neoformans) serotypes B and C (C neoformans var gattii).

Epidemiology n n Most cases of cryptococcosis are from serotypes A and D. Serotypes

Epidemiology n n Most cases of cryptococcosis are from serotypes A and D. Serotypes B and C are restricted to tropical and subtropical areas and are isolated from certain species of eucalyptus trees and the air beneath them. C neoformans var neoformans, which is recovered from aged pigeon feces, bird nests, and guano, invariably is serotype A or D. Although serotypes A and D occur in high concentrations in the pigeon feces, the fungus does not infect the birds.

n n n In moist or desiccated pigeon excreta, C neoformans may remain viable

n n n In moist or desiccated pigeon excreta, C neoformans may remain viable for 2 years or longer. In saprobic environments, C neoformans grows unencapsulated; however, unencapsulated strains regain their virulence following reacquisition of their polysaccharide capsule. C neoformans var gattii usually causes disease in patients with intact cellmediated immunity.

n n Naturally occurring cryptococcosis occurs in both animals and humans, but animalto-human transmission

n n Naturally occurring cryptococcosis occurs in both animals and humans, but animalto-human transmission or person-toperson transmission via the pulmonary route has not been documented. Transmission via organ transplantation has been reported when infected donor organs were used.

C neoformans var neoformans causes the vast majority of cryptococcal infections in hosts who

C neoformans var neoformans causes the vast majority of cryptococcal infections in hosts who are immunosuppressed, including patients with AIDS n C neoformans var gattii causes 7080% of cryptococcal infections occurring in hosts who are immunocompetent. n

n n No significant difference exists in the incidence of infection related to age,

n n No significant difference exists in the incidence of infection related to age, race, or occupation. Healthy persons with a history of exposure to pigeons or bird feces and laboratory workers exposed to an aerosol of the organism have a higher rate of positive delayed skin reaction to cryptococcal antigen or cryptococci.

Pathophysiology n n The organism primarily is transmitted via the respiratory route and not

Pathophysiology n n The organism primarily is transmitted via the respiratory route and not directly from one human to another. After inhaling C neoformans, the alveolar macrophages ingest the yeast. Phagocytosis and destruction of the unencapsulated yeast cells readily occur, whereas encapsulated organisms are more resistant to phagocytosis. A cryptococcal polysaccharide capsule has antiphagocytic properties and may be immunosuppressive.

The lack of identifiable endotoxins or exotoxins partly causes the absence of extensive necrosis

The lack of identifiable endotoxins or exotoxins partly causes the absence of extensive necrosis early in cryptococcal infections. n Well-formed granulomas generally are not present. n

n n If limited to the lungs, C neoformans infection may cause pneumonia, poorly

n n If limited to the lungs, C neoformans infection may cause pneumonia, poorly defined mass lesions, pulmonary nodules, and, rarely, pleural effusion. Although immune defects are common in patients with meningitis or disseminated infection, patients with disease that is confined to the lungs are usually immunocompetent.

Frequency approximately 7 -15% of patients with AIDS develop cryptococcal infections n AIDS-associated cryptococcal

Frequency approximately 7 -15% of patients with AIDS develop cryptococcal infections n AIDS-associated cryptococcal infections now account for 80 -90% of all patients with cryptococcosis n

Mortality/Morbidity Prior to the use of amphotericin B, cryptococcal meningitis and disseminated disease invariably

Mortality/Morbidity Prior to the use of amphotericin B, cryptococcal meningitis and disseminated disease invariably were fatal n 14% mortality rate in patients with cryptococcal disease who are treated with amphotericin B plus flucytosine n

History n n n Meningitis and meningoencephalitis are the most common manifestations and are

History n n n Meningitis and meningoencephalitis are the most common manifestations and are usually subacute or chronic in nature. This form of infection invariably is fatal without appropriate therapy; death may occur from 2 weeks to several years after the onset of symptoms. The clinical presentation and course of cryptococcal meningitis are variable, relating in part to underlying medical conditions (eg, diabetes, sarcoidosis, glucocorticoid use) and the immune status of the host.

n n The most common symptoms are headache and altered mental status, including personality

n n The most common symptoms are headache and altered mental status, including personality changes, confusion, lethargy, obtundation, and coma. Nausea and vomiting are frequent; fever and stiff neck are less common. Some patients who are HIV positive may have minimal or nonspecific symptoms at presentation. Patients are often afebrile or have a mildly elevated temperature.

Symptoms, including blurred vision, photophobia, and diplopia, may occur secondary to arachnoiditis, papilledema, optic

Symptoms, including blurred vision, photophobia, and diplopia, may occur secondary to arachnoiditis, papilledema, optic nerve neuritis, and chorioretinitis. n Other findings include hearing defects, seizures, ataxia, aphasia, and choreoathetoid movements. n Dementia is a potential sequela and may indicate the presence of hydrocephalus as a late complication. n

Physical n n Although C neoformans enters the body via the lungs, the CNS

Physical n n Although C neoformans enters the body via the lungs, the CNS is the main site of clinically evident infection in both immunocompetent and immunocompromised hosts. Immunocompetent hosts may present with either meningitis or focal cryptococcomas. Meningitis manifests with diffuse, nonfocal findings (eg, altered mental status, vomiting), whereas cryptococcomas often manifest with focal neurologic defects.

n Blood and CSF n n Even with widespread disease, the routine laboratory tests

n Blood and CSF n n Even with widespread disease, the routine laboratory tests (eg, leukocyte count, hematocrit, sedimentation rate) may produce normal results. Elevated opening pressure is associated with a poor prognosis. CSF glucose is depressed, the protein concentration is usually elevated, and the leukocyte counts are 20/m. L or higher, with lymphocytes generally outnumbering neutrophils. CSF can be normal at times, which is observed in patients with AIDS who are unable to mount an adequate inflammatory response or in persons with early asymptomatic infection.

n Smear and culture n n An India ink preparation is commonly used with

n Smear and culture n n An India ink preparation is commonly used with CSF to identify the organism and to support a presumptive diagnosis. If performed correctly, 25 -50% of patients with cryptococcal meningitis show cryptococci. Diagnosis depends on detecting the organism by culture; therefore, always confirm positive smears with cultures. Obtain urine and sputum cultures even if no clinical evidence of renal or pulmonary disease is present.

n n Positive blood culture results indicate extensive infection, and the organism may be

n n Positive blood culture results indicate extensive infection, and the organism may be observed within peripheral leukocytes or bone marrow macrophages in these patients. Use the lysiscentrifugation method of blood culture, which is the most sensitive and rapid. Whenever cryptococcosis occurs at any site, conduct a careful search for lesions elsewhere, both inside and outside the CNS.

n Serology n n Obtain a latex agglutination test to detect cryptococcal polysaccharide in

n Serology n n Obtain a latex agglutination test to detect cryptococcal polysaccharide in serum or CSF, which is an extremely important adjunct to the diagnosis. In patients with meningitis, cryptococcal antigen is positive in more than 90% and serum is positive in approximately 75%. Anticryptococcal antibodies do not have diagnostic significance, and low concentrations develop in a significant percentage of healthy people. Newer tests include monoclonal antibody–based latex agglutination and enzyme immunoassays, but experience with these tests is limited.

n Imaging Studies: n Prior to performing a lumbar puncture, conduct CT scanning or

n Imaging Studies: n Prior to performing a lumbar puncture, conduct CT scanning or MRI of the brain in patients who present with focal neurologic deficits or a history compatible with slowly progressive meningitis. If a mass lesion appears, do not perform a lumbar puncture to obtain spinal fluid; consult a neurosurgeon for an alternative procedure. In patients who are asymptomatic and immunocompetent, radiographic findings can include patchy pneumonitis, granulomas ranging from 2 -7 cm, or miliary disease similar to that observed in persons with tuberculosis. n n

Treatment n n Patients without AIDS Administering amphotericin B alone or in combination with

Treatment n n Patients without AIDS Administering amphotericin B alone or in combination with flucytosine may provide the appropriate therapy. Amphotericin B can be administered alone for 6 -10 weeks or in conjunction with flucytosine for 2 weeks, followed by fluconazole for a minimum of 10 weeks. Base therapy duration on CSF examination results.

n n Consider examining the patient's CSF weekly until culture conversion is documented and

n n Consider examining the patient's CSF weekly until culture conversion is documented and cultures remain negative for 4 weeks. In most cases, 6 -10 weeks of therapy is adequate. At the end of therapy, most patients have CSF glucose without abnormalities, but protein abnormalities may persist for years; therefore, do not allow this to dictate prolonging therapy.

Positive cultures persist or recur during active antifungal therapy in some patients. n The

Positive cultures persist or recur during active antifungal therapy in some patients. n The prostate may represent a sequestered focus of infection in men with recurrent disease. n

n n n Amphotericin B has a rapid onset of action and often leads

n n n Amphotericin B has a rapid onset of action and often leads to clinical improvement more rapidly than either intravenous or oral fluconazole. Because amphotericin B is nephrotoxic, monitor renal function carefully throughout its administration. Amphotericin B administered as a continuous infusion over 24 hours appears to have significantly less nephrotoxicity than the same doses administered over a 6 - to 8 -hour period.

n n Lipid formulations (eg, lipid complexes), liposome-associated amphotericin B, or amphotericin B colloidal

n n Lipid formulations (eg, lipid complexes), liposome-associated amphotericin B, or amphotericin B colloidal dispersion may be used in patients who do not respond to amphotericin B desoxycholate or who cannot tolerate its adverse effects, including nephrotoxicity. None of these alternative forms of amphotericin B is superior to standard nonlipid amphotericin B, and they all cost much more.

n n The lipid preparations may have an advantage in sparing renal function, but

n n The lipid preparations may have an advantage in sparing renal function, but they may be associated with higher relapse rates than amphotericin B desoxycholate. When used properly, standard amphotericin B–associated elevations in serum creatinine and BUN usually return to normal after therapy is completed.

n n n Flucytosine is unreliable if used alone, and resistance develops rapidly; in

n n n Flucytosine is unreliable if used alone, and resistance develops rapidly; in cryptococcal disease, administer this drug in conjunction with amphotericin B. Data on the use of fluconazole plus flucytosine are limited, but some investigators use this combination. If flucytosine is used with amphotericin B, pay careful attention to serum concentrations of flucytosine (which should be 25 -100 mcg/m. L), gastrointestinal toxicity, and bone marrow suppression.

Do not use currently available azoles (ketoconazole and itraconazole) in the initial treatment of

Do not use currently available azoles (ketoconazole and itraconazole) in the initial treatment of disseminated or CNS cryptococcal disease. n Azoles do not cross the blood-brain barrier adequately, and their onset of action is slower than amphotericin B. n

n n n Fluconazole is a bis-triazole that differs from other azoles by the

n n n Fluconazole is a bis-triazole that differs from other azoles by the substitution of a triazole group for the imidazole group. Because of the triazole substitution, fluconazole is water soluble and easily absorbed from the gut. Intravenous fluconazole can be used in early or mild disease; then, change to oral fluconazole in the same dose for 10 weeks to 2 years.

n n n Data regarding relapse with fluconazole are limited. Intravenous fluconazole may be

n n n Data regarding relapse with fluconazole are limited. Intravenous fluconazole may be administered to patients with cryptococcal meningitis, but its onset of action can be prolonged compared with that of amphotericin B Patients with AIDS and cryptococcal meningitis, oral fluconazole provides excellent long-term therapy once amphotericin B has controlled the acute meningitis.

Furthermore, fluconazole enters the prostate better than amphotericin B and can eradicate cryptococcal infection

Furthermore, fluconazole enters the prostate better than amphotericin B and can eradicate cryptococcal infection at this site. n Control of prostatic foci of cryptococcal yeast is important because relapses may occur if this site is not adequately treated. n

Thanks for your attention !!

Thanks for your attention !!