Case 4.

Демонстрация и обсуждение клинических случаев

Модераторы: Ren_Yumi, AOkhotin, Pyankov Vasily, Алексей Живов, Alon, dr.Ira

Ответить
Alon
Сообщения: 574
Зарегистрирован: Пн мар 19, 2007 11:19 pm
Откуда: Israel

Case 4.

Сообщение Alon »

Your secretary receives a frantic call from the mother of one of your patients: "My son is having a seizure and we're on the way to the emergency department!" The message is quickly relayed to you, and you pick up the young man's record in your office and page through it as you head to the ED. Quickly, the story comes back: a 17-year-old who had been well until 5 1/2 months ago, when he developed severe inflammatory bowel disease (IBD). The bloody diarrhea was initially managed with methylprednisolone sodium succinate (Solu-medrol), 100 mg (2 mg/kg) intravenously, twice a day for one month. Over the next month the Solu-medrol was switched to prednisone, orally, and then gradually tapered. A few days after completing the prednisone taper, his IBD flared and intravenous Solu-medrol was restarted, administered every six hours. After four days of Solu-medrol, he experienced a spontaneous, acute gastrointestinal bleed. A total colectomy and ileostomy were performed. After surgery, the Solu-medrol was changed to prednisone and tapered over the next two months. By coincidence, the young man was to have been seen in your office tomorrow for a six-week postoperative follow-up visit.

You meet the mother in the ED. Visibly shaken, she relates that the ED physicians saw her son's seizure upon arrival in the ED and that they described it as a right-sided focal seizure. She denies that he has had any fevers or recent cold symptoms. He is currently receiving no medications. There is no family history of seizures.

Once the young man's condition is stabilized, you proceed with your physical examination. You note that he is afebrile and that his other vital signs are unremarkable. He is now alert, and his mother feels that his mental status is back to normal. He tells you that the last thing he remembers is being at home in the kitchen and then awakening in the ED. The physical examination is also unremarkable, except for a few neurologic findings. There appears to be mild right facial and right upper extremity weakness. The deep tendon reflexes and sensory and cranial nerve examinations are normal, as is the rest of the neurologic examination.
------------------------------
The new onset of an afebrile seizure demands an evaluation.
Последний раз редактировалось Alon Чт апр 05, 2007 9:15 am, всего редактировалось 1 раз.
Всего наилучшего, Алон
internist
Сообщения: 45
Зарегистрирован: Чт мар 22, 2007 9:39 pm
Откуда: Украина

Сообщение internist »

ЭЭГ, электролиты сыворотки, возможно КТ/МРТ.
Alon
Сообщения: 574
Зарегистрирован: Пн мар 19, 2007 11:19 pm
Откуда: Israel

Сообщение Alon »

Although a cause cannot be found for the majority of seizures in adolescents, this young man's past history and the "sidedness" of his seizure suggest that the episode should not be neglected. Blood is sent for a complete blood count, serum chemistries, and culture; a urine toxicology screen is ordered. You also make arrangements for a magnetic resonance imaging (MRI) study of the head.
A ring to the diagnosis

A few hours later most of the laboratory tests have returned. The CBC and chemistries are unremarkable and the urine toxicology screen is negative. The call from the radiologist, however, substantiates one of your concerns; two lesions are found on the MRI scan. A 1.5 by 2 cm lesion is present in the pericentral gyrus, the posterior aspect of the left frontal lobe, which is enhanced by surrounding edema, and a similar lesion, 3 mm in size, is found in the left pontine area . The radiologist remarks that the lesions are atypical for a primary brain tumor and look like brain abscesses.
As you review the films with the radiologist you suspect that the months of steroid therapy may have set the young man up for the brain abscesses by rendering him immunocompromised. You also wonder if tuberculosis or a neoplasm could produce similar lesions. A chest X-ray and CT scans of the lungs and paranasal sinuses are ordered. A tuberculin skin test is placed, and a blood sample sent for human immunodeficiency virus testing. You also ask for oncology and neurosurgical consultations. Given the possibility of infection you decide to start ceftriaxone and metronidazole, the antibiotics of choice for treatment without a definite microbiologic diagnosis.

The oncologist feels that malignancy is unlikely in this patient, particularly in light of the MRI scan, and that a brain abscess is a better bet given the history of the prolonged course of steroids. The neurosurgeon is reluctant to biopsy the lesion, since surgical access would be through the motor cortex and there would be a risk of the young man losing function in his dominant right hand.

The chest X-ray and CT scans of the lungs and paranasal sinuses are read as normal. It does not look as if sinusitis or a pulmonary infection predisposed the young man to the abscess. The tuberculin skin test is negative at 48 hours, and the blood culture shows no growth. The HIV test is negative as well. In face of the presumptive diagnosis of brain abscess and considering the most likely organisms, you decide to continue the antibiotics for two months and follow the young man carefully.

Three months later the young man's neurologic symptoms are improved. The course of antibiotics was completed one month ago and the steroid taper a month before that. It looks as if he has responded nicely. Repeat MRI scans two, five, and eight weeks after antibiotics were started showed decreasing size of the brain lesions.

The next day, three months after the frantic call to your office about the seizure, comes another call with the same story. The seizures have returned! An MRI is scheduled as soon as possible. The pontine lesion appears to have resolved.The left frontal lesion has increased in size and the surrounding edema remains.
Всего наилучшего, Алон
Маша
Сообщения: 498
Зарегистрирован: Пт мар 30, 2007 9:30 pm
Откуда: Петербург

Сообщение Маша »

...Прямо детективная история.... :shock:
Я думаю надо сделать иммунограмму ,консультация онколога повторно ,повторить анализ на ВИЧ. Осмотр стоматолога...
Ведь откуда то инфекция попадает?
Дренирование абсцесса?
Alon
Сообщения: 574
Зарегистрирован: Пн мар 19, 2007 11:19 pm
Откуда: Israel

Сообщение Alon »

The neurosurgeon is consulted once again. In face of the apparent lack of response of the brain abscess to the two-month course of antibiotics a brain biopsy is needed to guide further therapy.

The young man undergoes a frontal craniotomy for biopsy of the lesion. A 2-cm, well-organized abscess is identified and completely excised. Later that afternoon the pathology laboratory calls to report that the abscess material contains hyphae that are septate and exhibit dichotomous, 45° angle branching. Your initial response to the laboratory call is dampened shortly thereafter by a report that the material that had been submitted for culture has been lost.

It looks like therapy will need to be determined on the basis of the fungus most likely to have caused the infection. Fungi with septated hyphae include Aspergillus species, Pseudallescheria boydii, and Fusarium species. The three cannot be easily distinguished on tissue sections. Aspergillus is a ubiquitous organism and the second most common cause of invasive fungal infection in patients with cancer and AIDS. In patients with cerebral aspergillosis who do not have an underlying immunosuppressive disease, symptoms are focal (headache, hemiparesis) and reflect the anatomic distribution of the underlying lesion. Brain abscesses caused by Aspergillus tend to localize in the frontal lobe, as a result of either hematogenous spread or direct extension from the paranasal sinuses. On histologic examination of surgical specimens, vascular invasion with infarction of surrounding tissues is typically present. Granuloma formation in the central nervous system is generally seen only in patients with prolonged aspergillosis.

Regardless of the patient's immunologic status, amphotericin B is the initial drug of choice for the treatment of cerebral aspergillosis. Liposomal amphotericin B, which accumulates in the reticuloendothelial system and is concentrated in the liver, spleen, lungs, and lymph nodes rather than the kidneys, is indicated only if a patient is unable to tolerate conventional amphotericin B or has an infection unresponsive to conventional amphotericin B. The crude mortality rate for cerebral aspergillosis in patients with and without primary immunosuppressive disease is 99% and 13%, respectively. This report leaves you with a sinking feeling.

Infections with Fusarium species are less likely to result in invasive disease than are those with Aspergillus, even in children with cancer. Brain abscesses are rare with Fusarium; more commonly these fungi present with lung infiltrates, sinusitis, or metastatic skin lesions. Amphotericin B has poor antifungal activity against all Fusarium species. Disease outcome improves with neutrophil recovery or complete excision of localized infections.

P boydii is found in soil, water, and the feces of farm animals. This opportunistic pathogen may cause infection in healthy and immunocompromised individuals. Respiratory infection, sinusitis, or osteomyelitis develop following accidental trauma with aspiration, inhalation, or bone penetration of contaminated soil. Brain abscesses with P boydii are exceedingly rare.6Miconazole is the drug of choice for treatment of infection with this organism.

The major risk factors for systemic fungal infections in immunocompromised hosts are neutropenia and corticosteroids. It seems clear that this young man had become immunocompromised during the prolonged course of corticosteroids used to treat his IBD, which included two courses of high-dose Solu-medrol. Based on his clinical picture, particularly the focal seizures and focal neurologic deficits, and the fact that Aspergillus organisms are ubiquitous and are far more likely to cause opportunistic infections than P boydii or Fusarium species, cerebral aspergillosis is presumed to be the most likely cause of his abscess. Amphotericin B is administered intravenously for two weeks and then for an additional week as itraconazole is begun orally. Itraconazole is continued for a total of six weeks.

Fortunately, the young man improves nicely. An MRI scan two months after he finishes antibiotic therapy shows complete resolution of the frontal lesion. At a two-year follow-up visit, only minimal right upper extremity weakness is noted. His survival despite delayed initiation of antifungal therapy was likely due to the discontinuation of immunosuppressive therapy and restoration of an immunocompetent state and, later, by the complete excision of a well-encapsulated abscess.

Although invasive fungal disease is most likely to occur in children with cancer and AIDS, opportunistic infections may also show up in children who are transiently immunosuppressed, including infants with bronchopulmonary dysplasia, children with severe asthma or renal disease, and children with IBD, particularly those who have required long courses of steroids to treat their maladies. We need to keep tabs on corticosteroids administered, keeping in mind immunosuppression and the unwelcomed and unlikely guests that may come with it. These are no fun guys to be around!
Всего наилучшего, Алон
Ответить