Very difficult question of pituitary apoplexy. It is a marginal topic in the MIR and also the answer is complex. Eliminating answers we are left with intervene (answer 4) or not to intervene (answer 2). In patients with hemodynamic instability, decreased level of consciousness, decreased visual acuity and extensive visual field defects, surgical decompression is recommended in the first week after symptom onset. I think the answer is 4, although it is oddly worded. I don't know if the neurosurgeon will support my answer.

Very difficult question of pituitary apoplexy. It is a marginal topic in the MIR and also the answer is complex. Eliminating answers we are left with intervene (answer 4) or not to intervene (answer 2). In patients with hemodynamic instability, decreased level of consciousness, decreased visual acuity and extensive visual field defects, surgical decompression is recommended in the first week after symptom onset. I think [HIDDEN], although it is oddly worded. I don't know if the neurosurgeon will support my answer.

A 63-year-old woman comes to the emergency department reporting severe headache with signs of meningeal irritation, bilateral visual disturbances and ophthalmoplegia. A CT scan showed a 2 cm space-occupying lesion in the sella turcica compatible with pituitary adenoma with signs of intratumoral hemorrhage, with deviation of the pituitary stalk and compression of the glandular tissue. Mark which of the following answers is WRONG:

Diagnostic suspicion is pituitary apoplexy.

Treatment with high-dose corticosteroids should be initiated and the evolution observed, since this treatment could reduce the volume of the lesion and avoid intervention.

Treatment with glucocorticoids should be considered to avoid secondary adrenal insufficiency that would compromise the patient's vital prognosis.

The presence of ophthalmoplegia and visual defects are indications for prompt intervention by urgent surgical decompression.

After resolution of the acute picture, the development of panhypopituitarism is frequent.

Presenting Symptoms of Pituitary Apoplexy.

The classical term "pituitary apoplexy" (PA) describes a clinical syndrome usually characterized by abrupt onset of headache accompanied by neurologic and/or endocrinologic deterioration due to sudden expansion of a mass within the sella turcica as a result of hemorrhage or infarction within a pituitary tumor and adjacent pituitary gland. PA is a medical emergency and a difficult diagnosis to establish. Thus this article reviews the presenting symptoms of PA patients to help clinicians recognize or at least suspect this critical condition early on. PA commonly occurs in the setting of a preexisting adenoma, and several patients are unaware of its existence prior to the onset of apoplexy symptoms, which are mainly of a neurologic, ophthalmologic, and endocrinologic nature. Neurologic symptoms include sudden-onset severe headache and other symptoms of subarachnoid hemorrhage, symptoms from compression of the cavernous sinus contents, nausea/vomiting, impaired consciousness, and symptoms of meningeal irritation. Ophthalmologic symptoms include visual field defects, visual loss, diplopia, and ophthalmoplegia. Endocrinologic disturbances include pituitary adenoma symptoms, cortisol deficiency, panhypopituitarism, diabetes insipidus, and syndrome of inappropriate secretion of antidiuretic hormone. Magnetic resonance imaging is the imaging method of choice to aid the PA diagnosis. Its differential diagnoses include cerebrovascular accidents, infectious diseases, and other causes of endocrinologic imbalance. Transsphenoidal surgery is the treatment of choice, especially if there are associated visual abnormalities and ophthalmoplegia. Clinicians should be aware of the presenting symptoms because early diagnosis may reduce the morbidity and mortality of this neurosurgical emergency.

Classical pituitary tumour apoplexy: clinical features, management and outcomes in a series of 24 patients.

We retrospectively analysed the incidence, clinical presentation, endocrinological and radiological findings, medical and surgical management of pituitary apoplexy in our department (single-centre study), having a large experience in pituitary surgery. Among 1540 pituitary lesions, 24 patients presented with pituitary apoplexy. Their charts were retrospectively reviewed. The symptoms included headache (92%), nausea and vomiting (54%), visual deficit (50%), oculomotor paresis (54%) and/or an altered mental state (42%). Skull X-rays (n = 14) demonstrated an enlarged sella turcica in all cases; CT-scan and/or MRI always revealed a sellar and suprasellar expanding lesion. Panhypopituitarism was present on admission in 70% of the patients. Urgent therapeutic management included high-dose cortisone treatment in all but one patients and CSF drainage in three. Three patients were treated conservatively. Nine patients were operated on rapidly, within hours or a few days because of severe visual deficit and/or altered level of consciousness. Nineteen patients were operated by the trans-sphenoidal approach; one of them required a second operation by craniotomy. There were two deaths related to the illness and one to an ill-defined reason at 4 months. Among the other patients 95% made a good recovery. All but two patients required a substitutive treatment with adrenal (83%), thyroid (68%), gonadal (42%) and/or growth (16%) hormones. The preoperative visual deficits recovered in all but one patients (92%) whereas the oculomotor pareses improved in all but two patients (85%). In conclusion, pituitary tumour apoplexy is a rare event, complicating in our series 1.6% of 1540 pituitary adenomas. Even in severe cases, complete recovery is possible if the diagnosis is rapidly obtained and adequate management is initiated in time. Surgical results after trans-sphenoidal approach are in the majority of cases very satisfactory.

Management of pituitary apoplexy.

Pituitary apoplexy is a rare clinical syndrome caused by sudden haemorrhaging or infarction of the pituitary gland, generally within a pituitary adenoma. Headache of sudden and severe onset is the main symptom, associated with visual disturbances or ocular palsy. Signs of meningeal irritation or altered consciousness may complicate the diagnosis. Corticotropic deficiency (secondary adrenal failure) may be life-threatening if untreated. Computed tomography (CT) or magnetic resonance imaging (MRI) confirm the diagnosis by revealing a pituitary tumour with haemorrhagic and/or necrotic components: CT is most useful in the acute setting (24 - 48 h), MRI is useful for identifying blood components in the subacute setting (4 days to 1 month). Owing to the highly variable course of this syndrome and the limited individual experience, the optimal management of acute pituitary apoplexy is controversial. Some authors advocate early transphenoidal surgical decompression for all patients, whereas others adopt a more conservative approach for selected patients (those without visual acuity or field defects and with normal consciousness). Glucocorticoid treatment must always be initiated immediately, at a dose of hydrocortisone 50 mg every 6 h.

Adrenal and pituitary emergencies.

Although loss of normal pituitary function may be silent and asymptomatic, sudden loss of gland function (pituitary apoplexy) typically results in characteristic presentations. Sheehan's syndrome is the development of hypopituitarism after postpartum hemorrhage or shock. Patients with Sheehan's syndrome may have typical or atypical presentations based on the extent of pituitary gland destruction. Patients with typical symptoms fail to lactate after giving birth; subsequently these patients also develop symptoms and signs of hypopituitarism. Measuring the serum prolactin level after giving thyrotropin-releasing hormone is a reasonable first step in the diagnosis of this condition in patients who fail to lactate after giving birth. The diagnosis of hypopituitarism is delayed for up to 7 years in patients with atypical symptoms. Acute symptomatic failure of the pituitary gland (pituitary apoplexy) commonly occurs in patients who have asymptomatic pituitary tumors. Many patients with pituitary tumors do not have signs of abnormal endocrine gland secretion and have a normal appearance. Most patients have the following signs or symptoms: headache; acute disturbances in visual acuity or visual fields; ophthalmoplegia, and changes in the level of consciousness. The syndrome of pituitary apoplexy usually evolves over hours to days. Subarachnoid hemorrhage and acute bacterial meningitis are the two most important mimics of pituitary apoplexy. Intravenous steroids and prompt neurosurgical consultation are mandatory in cases of pituitary apoplexy since both steroids and surgery can improve vision. Testings for acute or chronic hypopituitarism is challenging in the Emergency Department setting; however, carefully chosen tests will aid in the subsequent early correct diagnosis after initial Emergency Department management.

An interesting case of a pituitary adenoma apoplexy mimicking an acute meningitis. Case report.

Apoplexy of a pituitary adenoma is a rare and under-diagnosed clinical occurrence. It results from either infarction or haemorrhage into an adenoma of the pituitary gland. Its clinical presentation more often includes rapid development of impaired consciousness, severe headache, visual disturbance and variable association of oculomotor nerve palsy. Meningeal irritation signs are considered very rare and usually not reported as presenting symptoms. A 33-year-old male suffered a pituitary macroadenoma apoplexy, clinically indistinguishable from an infectious meningitis at presentation. Three days after surgery, the patient developed a left ophthalmoplegia due to 3(rd) nerve palsy, which fully resolved within 2 months. A right pterional craniotomy was performed during which complete tumour removal was achieved. In conclusion the authors believe that, despite many reports in the literature, encouraging conservative management in pituitary apoplexy by administering intravenous steroids, surgery should be undertaken in order to avoid eventual visual field defects, relieve pituitary gland compression and prevent a possible recurrent apoplectic episode or tumor re-growth.

[Surgical treatment of pituitary apoplexy].

Hypophysis apoplexy is a clinical syndrome characterized by the sudden development of headache, visual disturbance, associated with nausea, vomiting, signs of meningeal irritation and ophthalmoplegia. The symptoms are caused by the hemorrhage of a hypophyseal adenoma. This leads to the swelling of the tumor and compression of the perisellar structures. The authors processed the clinical and pathological characteristics of 28 cases occurring among the patient material of the National Institute of Neurosurgery of the past 10 years. According to the experiences the most important factor of a successful treatment of hypophyseal apoplexy is an early diagnosis and quick admittance to an institute of neurosurgery of satisfactory conditions. Thereafter a steroid hormone therapy of large doses and decompression operation performed by transnasal-transsphenoidal approach leads in the majority of cases to recovery.

Pituitary Apoplexy.

Pituitary apoplexy, a rare clinical syndrome secondary to abrupt hemorrhage or infarction, complicates 2%-12% of pituitary adenomas, especially nonfunctioning tumors. Headache of sudden and severe onset is the main symptom, sometimes associated with visual disturbances or ocular palsy. Signs of meningeal irritation or altered consciousness may complicate the diagnosis. Precipitating factors (increase in intracranial pressure, arterial hypertension, major surgery, anticoagulant therapy or dynamic testing, etc) may be identified. Corticotropic deficiency with adrenal insufficiency may be life threatening if left untreated. Computed tomography or magnetic resonance imaging confirms the diagnosis by revealing a pituitary tumor with hemorrhagic and/or necrotic components. Formerly considered a neurosurgical emergency, pituitary apoplexy always used to be treated surgically. Nowadays, conservative management is increasingly used in selected patients (those without important visual acuity or field defects and with normal consciousness), because successive publications give converging evidence that a wait-and-see approach may also provide excellent outcomes in terms of oculomotor palsy, pituitary function and subsequent tumor growth. However, it must be kept in mind that studies comparing surgical approach and conservative management were retrospective and not controlled.

[Pituitary apoplexy: an endocrinologic emergency].

A 32-year-old woman, a 73-year-old man and a 26-year-old pregnant woman presented with headache, vomiting, and variable presence of visual disturbances, impaired consciousness, and circulatory shock. All three had pituitary apoplexy. In the first patient lymphocytic hypophysitis was diagnosed, the second had a nonfunctional adenoma and the last patient probably also. All three patients were treated conservatively with full recovery of signs and symptoms. However pituitary insufficiency remained in all three. Pituitary apoplexy is an acute event with significant morbidity and mortality. The cause is a rapid expansion of, usually, a pre-existing, often not yet known, adenoma by massive haemorrhage or infarction. Pressure, among other things, causes hypopituitarism, meningism, compression of the chiasma opticum and visual disturbances. Although many predisposing factors have been identified, pituitary apoplexy is often an unpredictable event. Diagnosis is made by the typical clinical presentation, eye examination, MRI and by measuring pituitary hormones. Treatment is with suppletion of the deficient hormones and in selected patients by transsphenoidal decompression surgery.

[Pituitary apoplexy].

Pituitary apoplexy results from necrosis or haemorrhage of a pituitary adenoma. This rare complication occurs in 2 to 10% of operated adenomas. The acute form results from massive intrapituitary bleeding leading to violent headache, meningeal signs, impaired conscience and ophthalmology signs, basically bilateral blindness. Associated signs are frequent including paralysis of the oculomotor nerves, epilepsy seizure, hemiplegia. Diabetes insipidis is exceptional. In less acute forms, the sudden nature of the headache and ophthalmology signs can suggest diagnosis. Standard X-ray reveals destruction of the sella turcica. Computed tomography shows either a haematoma or a cystic cavity in the pituitary gland which must be perfectly described together with the integrity of the bone structures due to the risk of lysis. Magnetic resonance imaging is an essential technique which can be used to describe the volume and suprasellar extension of the tumour, its texture, possible compression of adjacent structures and determine the age of the haemorrhage. This imaging technique can also isolate rare optochiasmatic apoplexia requiring intracranial evacuation. Emergency surgery is mandatory for most all authors. Rhinal-septal decompression is usually used, but the intracranial route may be preferred for very large suprasellar tumours. Medical treatment alone may be successful for small prolactin adenomas. Outcome depends on the time lapse to decompression. Optic nerve recovery is usually possible if the delay is less than 7 days. Cranial nerve recovery is less dependent on the time interval. In all cases hormone substitution is required.

An altered state of consciousness while using anticoagulants and the incidental discovery of a pituitary lesion: considering pituitary apoplexy.

Pituitary apoplexy (PA) is a medical emergency with complex diagnosis and management. In this study, we describe a case of PA in a 63-year-old male treated with oral anticoagulant therapy for atrial fibrillation. In the patient, PA manifested itself with asthenia and severe headache not responsive to common analgesics. Despite the finding of a pituitary mass through CT, and in anticipation of the endocrinological evaluation and pituitary MRI, the patient's clinical condition worsened with an escalation of headache and asthenia associated with deterioration of the visual field and impairment of consciousness level. The emergency assessments revealed an adrenal failure, whereas MRI showed a haemorrhagic pituitary macroadenoma with compression of the optic chiasm. Intravenous fluids repletion and high-dose hydrocortisone were started with a rapid improvement of the patient's health and visual field abnormalities. Hydrocortisone was gradually reduced to a replacement dose. During the follow-up, panhypopituitarism was documented, and replacement therapies with l-thyroxine and testosterone were introduced. Three months later, a pituitary MRI showed a 50% reduction in the pituitary adenoma volume. Pituitary apoplexy (PA) is a medical emergency that can result in haemodynamic instability and abnormalities in the level of consciousness. The management of PA requires a multidisciplinary team that includes endocrinologists, ophthalmologists, neuro-radiologists, and neuro-surgeons. Pituitary MRI with gadolinium is the diagnostic gold standard for PA. PA therapy aims to improve general conditions and treat compression symptoms, especially visual field abnormalities. Adrenocorticotrophic hormone deficiency is a common and severe complication of PA. Thus, all patients with PA must be promptly treated with injective synthetic glucocorticoids (e.g. hydrocortisone 100 mg) and i.v. saline. PA must be taken into consideration in case of sudden headache in patients with a pituitary macroadenoma, especially if other risk factors are recognized.

Complete surgical resolution of bilateral total opthalmoplegia without visual field defect in an acromegalic patient presented with pituitary apoplexy.

Pituitary apoplexy (PA), which is one of the most serious life-threatening complications of pituitary adenoma, is characterized by abrupt onset of headache, nausea, vomiting, visual disturbances and oculomotor paresis. Combination of oculomotor cranial nerve paralysis with normal visual fields is very rare in PA. We report a 60-year-old acromegalic man presented with panhypopituitarism and bilateral total opthalmoplegia without a visual field defect. At initial evaluation his clinical findings were compatible with adrenal crisis and eye examination revealed total opthalmoplegia, bilateral ptosis and normal vision. MRI showed a large heterogeneous mass in the pituitary fossa. Although clinical findings due to adrenal crisis improved after glucocorticoid therapy there was no improvement in opthalmoplegia and ptosis. The patient underwent transsphenoidal excision of the pituitary mass. Histological examination revealed an adenoma with large areas of hemorrhagic infarction and most of the cells were positive for GH in immunohistochemical analysis. Although opthalmoplegia was severe at presentation, total recovery was achieved 3 months after transsphenoidal surgery. Therefore the presented case clearly demonstrates that opthalmoplegia without a visual field defect due to PA has a good prognosis and early diagnosis and treatment including surgical decompression are crucially important.

Neurological Presentation of Giant Pituitary Tumour Apoplexy: Case Report and Literature Review of a Rare but Life-Threatening Condition.

Giant pituitary adenomas are benign intracranial tumours with a diameter ≥4 cm. Even if hormonally non-functional, they may still cause local extension, leading to symptoms that include mostly gland dysfunction, mass effects, and, much less frequently, apoplexy due to haemorrhage or infarction. Neurological presentation of giant pituitary tumour apoplexy is even more rare and has not been systematically reviewed. An 81-year-old woman was admitted to the Emergency Department because of acute onset headache, bilateral visual deficit, and altered consciousness. Computed tomography showed a giant mass lesion (&gt;5.5 cm diameter) expanding upward to the suprasellar cistern, optic chiasm, and third ventricle, over-running the sphenoid sinus, and with lateral invasion of the cavernous sinus. Laboratory investigations revealed central adrenal and hypothyroidism insufficiency, while magnetic resonance imaging confirmed a voluminous suprasellar tumour (~6 cm diameter), with signs of pituitary tumour apoplexy. Neurological manifestations and gland-related deficits improved after hormonal replacement therapy with a high dose of intravenous hydrocortisone, followed by oral hydrocortisone and levo-thyroxine. The patient declined surgical treatment and follow-up visit. Giant pituitary tumour apoplexy is a rare but potentially life-threatening condition. Prompt diagnosis and multidisciplinary management may allow a remarkable clinical improvement, as seen in this case.

Hypothalamitis: a diagnostic and therapeutic challenge.

To report an unusual case of biopsy-proven autoimmune hypophysitis with predominant hypothalamic involvement associated with empty sella, panhypopituitarism, visual disturbances and antipituitary antibodies positivity. We present the history, physical findings, hormonal assay results, imaging, surgical findings and pathology at presentation, together with a 2-year follow-up. A literature review on the hypothalamic involvement of autoimmune hypophysitis with empty sella was performed. A 48-year-old woman presented with polyuria, polydipsia, asthenia, diarrhea and vomiting. The magnetic resonance imaging (MRI) revealed a clear suprasellar (hypothalamic) mass, while the pituitary gland appeared atrophic. Hormonal testing showed panhypopituitarism and hyperprolactinemia; visual field examination was normal. Pituitary serum antibodies were positive. Two months later an MRI documented a mild increase of the lesion. The patient underwent biopsy of the lesion via a transsphenoidal approach. Histological diagnosis was lymphocytic "hypothalamitis". Despite 6 months of corticosteroid therapy, the patient developed bitemporal hemianopia and blurred vision, without radiological evidence of chiasm compression, suggesting autoimmune optic neuritis with uveitis. Immunosuppressive treatment with azathioprine was then instituted. Two months later, an MRI documented a striking reduction of the hypothalamic lesion and visual field examination showed a significant improvement. The lesion is stable at the 2-year follow-up. For the first time we demonstrated that "hypothalamitis" might be the possible evolution of an autoimmune hypophysitis, resulting in pituitary atrophy, secondary empty sella and panhypopituitarism. Although steroid treatment is advisable as a first line therapy, immunosuppressive therapy with azathioprine might be necessary to achieve disease control.

Management of endocrine disease: pituitary tumour apoplexy.

Pituitary tumour apoplexy (PA) is a rare clinical syndrome that occurs as a result of acute haemorrhage and/or infarction within a frequently undiagnosed pituitary tumour. The sudden enlargement of the pituitary mass undergoing PA is responsible for a wide range of acute symptoms/signs (severe headache, visual loss, diplopia, hypopituitarism, impaired consciousness) which, together with the radiological evidence of a pituitary lesion, establish the diagnosis. The optimal care of PA requires involvement of a multidisciplinary team including endocrinologist, neurosurgeon, neuroophthalmologist and the management strategy that depends on the clinical manifestations, as well as the presence of co-morbidities. Prompt surgical decompression is initially indicated in cases with severe or progressive impairment of the visual acuity or the visual fields or with altered mental state and leads to visual and neurological recovery in most of the patients. The patients with mild, stable clinical picture (including those with isolated ocular palsies) can be managed conservatively (support of fluid and electrolyte balance and stress doses of steroids in most cases) with favourable visual and neurological outcome. Frequent reassessment is mandatory because the clinical course can be unpredictable; if progression of symptoms occurs, later elective surgery is indicated and is beneficial, especially in terms of visual outcome. The endocrinological outcome is less favourable, irrespective of the treatment option, with many patients remaining on long-term replacement therapy. Despite the above guidelines, clear proof of optimal outcomes in the form of randomised controlled trials is lacking. Regrowth of the pituitary tumour years after a PA episode is possible and patients require long-term surveillance.

Improvement of pituitary function after surgical decompression for pituitary tumor apoplexy.

Hypopituitarism is a major manifestation of pituitary adenoma apoplexy. We postulated that the acute deterioration in pituitary function may be caused by compression of portal vessels and the pituitary stalk, secondary to a sudden increase in intrasellar contents. If this were the case, one would predict improvement in pituitary function to occur after surgical decompression. We studied pituitary function in eight patients presenting with the clinical syndrome of pituitary adenoma apoplexy before and on multiple occasions after urgent surgical decompression. Partial or complete hypopituitarism was seen in all subjects at the time of presentation. Serum cortisol levels were inappropriately low (5.9 +/- 1.4 micrograms/dL; 162.8 +/- 38 nmol/L) for the degree of stress in seven patients and appropriately elevated in only one subject (55.3 micrograms/dL; 1525.7 nmol/L). High normal increments in cortisol levels were noted in three subjects given test doses of cosyntropin. Patients were given glucocorticoids before, during, and for 2 days after surgery. Serum cortisol concentrations measured on or after the third day when glucocorticoids had already been stopped were normal in seven subjects and consistently low in one. These seven subjects were discharged on no replacement and were subsequently documented by dynamic testing to have normal pituitary-adrenal function. Gonadal function improved in two of four men and in one of two women who had hypogonadism on presentation. Improvement in thyroid function was documented in two of three subjects with preoperative hypothyroidism. Gradual improvement and almost complete resolution of the neuroophthalmological abnormalities occurred days to weeks after decompression. These observations demonstrate that urgent surgical decompression after pituitary tumor apoplexy was associated with improvement not only in neurological defects but also in pituitary function. The rapid improvement in pituitary function indicates not only that the hypopituitarism was reversible, but also that it might be caused by compression of the portal circulation and pituitary stalk by the sudden increase in intrasellar contents.

Gestational pituitary apoplexy: Case series and review of the literature.

Pituitary apoplexy is an uncommon but potentially life-threatening emergency due to abrupt ischemic infarction or hemorrhage of the pituitary tumor. In many instances, pituitary apoplexy is the initial presentation in patients who were not previously diagnosed to have pituitary adenomas. Variety of precipitating factors have been linked to the occurrence of pituitary apoplexy, which include pregnancy. However, pituitary apoplexy related to pregnancy is limited to isolated case reports and very small case series. The main symptom is headache of sudden onset associated with visual disturbances, signs of meningeal irritation, and/or endocrine dysfunction. In the context of pregnancy the diagnosis of pituitary apoplexy can be challenging and confused with other complex conditions such as pre-eclampsia. Magnetic resonance imaging is the most sensitive sequence to confirm the diagnosis by revealing a pituitary tumor with hemorrhagic and/or necrotic components. Corticotropic deficiency with adrenal insufficiency is a potentially life-threatening disorder for both mother and the fetus if left untreated. The choice between conservative management with dopamine agonists and glucocorticoid, this "wait and see approach" and trans-sphenoidal resection depend on the severity of neuro-ophtalmic signs and the gestational week. In this article, we present three cases of pituitary apoplexy related to pregnancy. Pituitary apoplexy occurred in the third trimester in the three cases. It was the first presentation of an unknown pituitary adenoma in two cases, and complicated a preexisting macroprolactinoma in the other case. All three cases of our patients had sudden onset of severe headache and deterioration of the visual field in two cases. The pituitary MRI performed in our patients was the essential tool confirming the diagnosis of pituitary apoplexy. In all the patients was prompt replacement of deficient hormones especially glucocorticoids with close surveillance. The trans-sphenoidal resection was indicated in two pregnant women; as the first choice treatment in one case presenting with papillary edema, and as the second line after the deterioration of the visual field in one case. In the lack of guidelines of management pituitary apoplexy in case of pregnancy, we review the existing literature with pertinent clinical presentation, radiological findings, management and maternal/fetal outcomes of this rare pathology. The aim is to provide a rational framework for therapeutic management of pituitary apoplexy during pregnancy.

[Adenomatous hypophyseal apoplexy. Clinical, diagnostic and therapeutic aspects of a frequently misdiagnosed emergency state].

Pituitary adenoma apoplexy was considered an acute life-threatening condition until more benign and even asymptomatic courses were found by advanced neuroimaging procedures. Necrosis and hemorrhage in the pituitary adenoma can cause acute enlargement of the tumor. sometimes with rupture of the tumor capsule and bleeding into the subarachnoid space and surrounding parts of the brain. Clinical symptoms include acute or subacute headache in combination with signs of meningeal irritation and neuroophthalmological and cerebral dysfunction. Severe panhypopituitarism may be an additional complication. Acute blindness due to compression of the optic chiasm and symptomatic compression of basal cerebral arteries require immediate transsphenoid tumor resection. If panhypopituitarism is suspected, immediate hormone substitution is necessary.

Pituitary apoplexy

Pituitary apoplexy is bleeding into or impaired blood supply of the pituitary gland. This usually occurs in the presence of a tumor of the pituitary, although in 80% of cases this has not been diagnosed previously. The most common initial symptom is a sudden headache, often associated with a rapidly worsening visual field defect or double vision caused by compression of nerves surrounding the gland. This is often followed by acute symptoms caused by lack of secretion of essential hormones, predominantly adrenal insufficiency. The diagnosis is achieved with magnetic resonance imaging and blood tests. Treatment is by the timely correction of hormone deficiencies. In many cases, surgical decompression is required. Many people who have had a pituitary apoplexy develop pituitary hormone deficiencies and require long-term hormone supplementation. The first case of the disease was recorded in 1898. Signs and symptoms

Pituitary apoplexy.

Pituitary apoplexy is a clinical syndrome of headache, visual deficits, ophthalmoplegia, and alteration in mental status resulting from the sudden hemorrhage or infarction of a pituitary adenoma. Infarction of a normal gland also may occur in certain circumstances. Its manifestations are variable, ranging from a clinically benign event to a catastrophic presentation with permanent neurologic deficits or even death. It frequently mimics other intracranial processes and, without a high index of suspicion, may be difficult to diagnose. Radiographic studies, particularly CT and MR imaging, are helpful for diagnosis in both the acute and subacute settings. In its most fulminant presentation, prompt neurosurgical decompression is necessary to preserve sight and life. Corticosteroid replacement is also essential in the acute phase because of the high incidence of adrenal insufficiency. Fortunately, however, with proper management most patients may have good outcomes.

Pituitary adenoma

Pituitary apoplexy is a condition that occurs when pituitary adenomas suddenly hemorrhage internally, causing a rapid increase in size or when the tumor outgrows its blood supply which causes tissue necrosis and subsequent swelling of the dead tissue. Pituitary apoplexy often presents with visual loss and sudden onset headache and requires timely treatment often with corticosteroids and if necessary surgical intervention. Central diabetes insipidus is caused by diminished production of the antidiuretic hormone vasopressin that causes severe thirst and excessive production of very dilute urine (polyuria) which can lead to dehydration. Vasopressin is produced in the hypothalamus and is then transported down the pituitary stalk and stored in the posterior lobe of the pituitary gland which then secretes it into the bloodstream.

[Pituitary abscess, treated by medication].

Pituitary abscesses are rare. The case reported here concerns a 28-year old African. Gradual development of diplopia over 6 months was the first clinical manifestation. Three months later this development had reached a more severe and infectious context, with complete right ophthalmoplegia, meningitis and coma (GCS = 9). CT scan showed an image in favour of a pituitary abscess with suprasellar extension, associated with thrombophlebitis of the cavernous sinus. An antibiotic therapy consisting of cefotaxime and metronidazole administered for 1 month, and netilmicin for 15 days succeeded in controlling the infectious syndrome. This resulted in cure of visual disorders, reduction in size of the CT scan image and reconstruction of the pituitary sella which had been destroyed. The diagnosis of pituitary abscess should be made when confronted with an infectious syndrome (unexplained fever, repeated meningitis). CT does not recognize the nature of the hypophyseal mass it shows: necrosis of a pituitary adenoma, giant aneurysm or craniopharyngioma may mimic local infection. Surgery confirms the diagnosis and is regarded as the best treatment. The patient's life is threatened when meningitis is present, and the functional prognosis is poor when recovery from visual disorders is compromised due to late diagnosis. In this paper a comparative analysis of the clinical course of the disease and therapeutic data in our patient is presented and compared with other reported cases.

[Clinical practice guideline for the diagnosis and treatment of pituitary apoplexy].

Classic pituitary apoplexy (PA) is an acute, life-threatening clinical syndrome caused by acute hemorrhage and/or infarction of the pituitary gland. PA is considered a neuroendocrinological emergency. However, there is no consensus about the best options for PA diagnosis and management. To develop a clinical practice guideline with a number of recommendations for diagnosis and treatment of patients with PA based on the medical evidence available, in order to help clinicians involved in their care. The clinical guideline for diagnosis and treatment of pituitary apoplexy issued in 2006 by the Neuroendocrinology Working Group of the Spanish Society of Endocrinology and Nutrition (SEEN) and the British Clinical Practice Guideline published in 2011 were taken as the basis. The text has been adapted to the format used in most international medical journals. For this, after updated medical literature, the quality of evidence and the strength of the recommendations were evaluated using the system proposed by the Agency for Health Care Policy and Research (AHCPR). Diagnosis of pituitary apoplexy should be considered in all patients with acute severe headache with or without neuro-ophthalmic signs. Patients with PA must undergo a complete history and physical examination. All patients with suspected pituitary apoplexy should have urgent blood samples drawn to test electrolytes, renal function, liver function, coagulation screen, complete blood count, and basal levels of pituitary and peripheral hormones, and to rule out adrenocorticotropic hormone (ACTH) deficiency. Formal visual field assessment should be performed when the patient is clinically stable. Magnetic resonance imaging (MRI) is the imaging test of choice to confirm diagnosis. Indications for empirical urgent corticosteroid therapy in patients with PA include hemodynamic instability, impaired consciousness, reduced visual acuity, and severe visual field defects. In patients with these severe neuro-ophthalmic signs, surgery should be considered. Surgery should preferably be performed within seven days of the onset of symptoms. Patients with mild and stable signs may be managed conservatively with careful monitoring. Treatment and long-term follow-up of patients with PA should be conducted by a multidisciplinary team consisting, amongst others, of an experienced pituitary neurosurgeon, an ophthalmologist, and an endocrinologist.

Pituitary apoplexy, therapeutic assessment.

The management of pituitary apoplexy with reference to both diagnosis and operative sequelae remains a major challenge. Acute onset of retro-orbital headache in association with visual loss and ophthalmoplegia are the cardinal symptoms; however, obtundation and signs of subarachnoid hemorrhage also may be present. Good quality plain skull radiographs and complete angiography prove sufficient for preoperative radiographic studies. Preoperative endocrine preparation focuses on supplemental glucocorticoids since these patients must be presumed deficient in cortisol reserve. Residual visual deficit appears to be more a function of the extent of damage at the time of ictus rather than rapidity of decompression. Our experience indicates that transsphenoidal decompression in appropriate cases offers an ideal opportunity to minimize mortality and morbidity. The acute onset of severe retro-orbital headache in association with stupor and ocular palsies would alert most physicians to the potential diagnosis of spontaneous subarachnoid hemorrhage. The association of complex ophthalmoplegias and visual defects in this constellation of symptoms should, in addition, alert one to the possibility of an acute intrasellar or parassellar expansile process. During the past two years, we have had the opportunity to care for 8 such patients with confirmed diagnoses of acute hemorrhagic infarction of the pituitary enabling us to formulate diagnostic and therapeutic schemata with reference to management of this problem.

Management and outcomes of pituitary apoplexy.

This study was undertaken to analyze the predisposing factors, clinical presentation, therapeutic management, and clinical recovery in patients with pituitary apoplexy, with an emphasis on the long-term visual, endocrine, and functional outcomes. The authors performed a retrospective analysis of consecutive cases involving patients treated at Mayo Clinic between 1992 and 2013. Patients were included in the study only if they had 1) abrupt onset of severe headache or visual disturbance in the presence of a pituitary adenoma and 2) radiological or surgical confirmation of a pituitary mass. The primary endpoints of analysis were the visual (ocular motility, visual fields, and visual acuity), endocrine, and functional outcomes (using the modified Rankin Scale). Eighty-seven patients were identified (57 males and 30 females, mean age 50.9 years, range 15-91 years). Twenty-two patients (25.3%) had a known pituitary adenoma. Hypertension was the most common associated factor (39%). Headache was the most frequent presenting symptom (89.7%), followed by visual abnormalities (47.1%). Cranial nerve palsies were present in 39% and visual field defects in 34.1%. MRI detected hemorrhage in 89% patients, as compared with 42% detected by CT scan. Sixty-one patients (70.1%) underwent surgery during acute hospitalization (median time from apoplexy 5 days, IQR 3-10 days), 8 (9.2%) had delayed surgery, and 18 (20.7%) were treated conservatively. Histopathological examination revealed adenoma with pure necrosis in 18 (30%), pure hemorrhage in 4 (6.7%), and both in 6 (10%) patients. Four patients died during hospitalization. The average duration of follow-up was 44.2 ± 43.8 months. All survivors were independent and had complete resolution or substantial improvement in eye movements and visual fields at the last follow-up. Many patients needed long-term hormonal replacement with levothyroxine (62.7%) and cortisol (60%). Daily desmopressin was needed in 23% of all surgical patients at 3 months (versus none of the medically treated) and this requirement decreased slightly over time. Regrowth of pituitary adenoma was seen in 7 patients (8.6%). There were no statistically significant differences in any of the outcome measures across the treatment groups. The outcome of most patients with pituitary apoplexy is excellent. Selected patients can be managed conservatively, and patients with severe neuro-ophthalmological deficits treated with early surgery can achieve an excellent recovery.

Pituitary Apoplexy Following Systemic Anticoagulation.

Pituitary apoplexy is a rare medico-surgical emergency that stems from an acute expansion of a pituitary adenoma from infarction or haemorrhage and where the treatment strategy is still controversial. Clinical presentation is highly variable and a high index of suspicion is needed to make the diagnosis. Furthermore, in less than half of cases, a precipitating event is identified. We report a case of a 74-year-old female who, after introduction of anticoagulation for pulmonary thromboembolism, presented with pituitary apoplexy heralded by acute adrenal insufficiency, headaches, visual symptoms and hypogonadotropic hypogonadism. Timely initiation of corticosteroids was crucial, and after stabilisation, a conservative treatment strategy was favoured with good long-term prognosis. Long-term follow-up of pituitary function also revealed new growth hormone deficiency. Corticosteroid therapy may be crucial in the emergency setting, and it is recommended for all patients with suspected pituitary apoplexy (PA).Early recognition of PA and its predisposing factors is crucial for the best outcome for the patient.Initial conservative treatment strategies are gaining popularity but close clinical monitoring is fundamental to recognise the need for sellar decompression.

Pituitary adenoma

Ectopic pituitary adenoma An ectopic (occurring in an abnormal place) pituitary adenoma is a rare type of tumor which occurs outside of the sella turcica, most often in the sphenoid sinus, suprasellar region, nasopharynx and the cavernous sinuses. Metastases to the pituitary gland Carcinomas that metastasize into the pituitary gland are uncommon and typically seen in the elderly, with lung and breast cancers being the most prevalent, In breast cancer patients, metastases to the pituitary gland occur in approximately 6-8% of cases. Symptomatic pituitary metastases account for only 7% of reported cases. In those who are symptomatic Diabetes insipidus often occurs with rates approximately 29-71%. Other commonly reported symptoms include anterior pituitary dysfunction, visual field defects, headache/pain, and ophthalmoplegia.

InternalMed_Harrison

Pituitary Apoplexy Acute intrapituitary hemorrhagic vascular events can cause substantial damage to the pituitary and surrounding sellar structures. Pituitary apoplexy may occur spontaneously in a preexisting adenoma; postpartum (Sheehan’s syndrome); or in association with diabetes, hypertension, sickle cell anemia, or acute shock. The hyperplastic enlargement of the pituitary, which occurs normally during pregnancy, increases the risk for hemorrhage and infarction. Apoplexy is an endocrine emergency that may result in severe hypoglycemia, hypotension and shock, central nervous system (CNS) hemorrhage, and death. Acute symptoms may include severe headache with signs of meningeal irritation, bilateral visual changes, ophthalmoplegia, and, in severe cases, cardiovascular collapse and loss of consciousness. Pituitary computed tomography (CT) or MRI may reveal signs of intratumoral or sellar hemorrhage, with pituitary stalk deviation and compression of pituitary tissue.

InternalMed_Harrison

Patients with no evident visual loss or impaired consciousness can be observed and managed conservatively with high-dose glucocorticoids. Those with significant or progressive visual loss, cranial nerve palsy, or loss of consciousness require urgent surgical decompression. Visual recovery after sellar surgery is inversely correlated with the length of time after the acute event. Therefore, severe ophthalmoplegia or visual deficits are indications for early surgery. Hypopituitarism is common after apoplexy.

Clinical and imaging features of pituitary apoplexy and role of imaging in differentiation of clinical mimics.

To discuss the clinical syndrome, review common imaging findings of pituitary apoplexy (PA) and role of imaging in therapy and follow-up. Also, to review other acute clinical scenarios with similar clinical and/or imaging findings as PA. PA is a severe and potentially life-threatening medical emergency, characterized by constellation of symptoms/signs that occur as a result of acute hemorrhage and/or infarction in pituitary gland. Patients present with acute and sudden onset of symptoms/signs, most commonly with severe headache, vision deficits/ophthalmoplegia, altered mental status, and possible pan hypopituitarism. Pre-existing macro adenoma (65-90%), especially non-functioning and prolactinomas, are most susceptible to apoplexy, which undergoes hemorrhage or infarct, but PA can occur with normal pituitary or microadenoma. Because of the probable grave prognosis of PA, imaging characteristics of PA and other acute clinical scenarios with similar clinical and/or imaging findings should be familiar to radiologists. PA is potentially a life-threatening clinical syndrome, however, imaging and clinical findings can lead the radiologist towards appropriate diagnosis, and rule out other clinical mimics. When hemorrhage is secondary to an underlying lesion, regrowth of the pituitary tumor years after a PA episode is possible and patients require long-term clinical and imaging surveillance.

Pituitary Apoplexy -- Treatment / Management

Management of the mass is controversial as some advocate early transsphenoidal surgical decompression in all patients, whereas others adopt a conservative approach for those patients without visual acuity or field defects and with normal consciousness. Emergency surgery should be reserved for patients with progressive deterioration of consciousness, hypothalamic involvement, and progressive visual worsening. It has been demonstrated that a significant postoperative clinical improvement is a consequence of a surgical procedure performed as soon as possible. [23] Decompressive surgery can be delayed but performed within 1 week when visual acuity defects appear stable. If ophthalmoplegia is improving or stable, a conservative strategy could be considered. [34] [35] Microscopic endonasal or sublabial transsphenoidal surgery is commonly used. For very large tumors and those extending over the chiasm or laterally to the temporal fossa, a craniotomy should be used to achieve complete resection. Endoscopic endonasal approaches for pituitary apoplexy are effective. [30] [36] [37] Patients operated using the endoscopic approach have a similar visual outcome, but a better endocrinological outcome as the viable tumoral component can be removed from restricted areas like the cavernous sinus. [38] Sometimes, an endoscopic approach can prove difficult to perform if required at late night hours as it needs the collaboration of an otolaryngologist with the neurosurgeon.

Acute sterile meningitis as a primary manifestation of pituitary apoplexy.

Pituitary apoplexy is a rare and underdiagnosed clinical syndrome. It results from hemorrhagic infarction of the pituitary gland. In its classical form it is characterized by acute headache, ophthalmoplegia, visual loss and pituitary insufficiency. Meningeal irritation signs, clinically indistinguishable from infectious meningitis, are considered rare and have not been reported as presenting signs. We report a 53-yr-old man who was admitted to hospital following acute headache, fever, neck stiffness and paresis of the left oculomotor and abducent nerves. A lumbar puncture revealed an increased number of polymorphs but with a sterile cerebral spinal fluid. Magnetic resonance imaging (MRI) showed an intrasellar mass with central necrosis in an enlarged sella. Endocrinological evaluation demonstrated insufficient thyroid, adrenocortical, and gonadal function. Necrosis within a chromophobe adenoma was found upon surgical decompression of the sella. After surgery anterior panhypopituitarism did not recover, while ophthalmoplegia subsided. The patient is now in good health under appropriate hormonal replacement therapy.

Corticosteroid treatment buys time in case of a newly diagnosed hypophysitis with visual deterioration.

Hypophysitis is an important differential diagnosis for a pituitary mass, especially in young women at the end of or shortly after pregnancy. It commonly results in hypopituitarism and can be differentiated from adenoma on MRI. Typical MRI characteristics of hypophysitis are symmetry, loss of posterior bright spot, intense and homogeneous gadolinium enhancement, a thickened pituitary stalk and intact sellar floor. Treatment of choice in the acute phase of a hypophysitis is corticosteroids. Adequate corticosteroid treatment may effectively buy time and avoid unnecessary surgical treatment and is related to further decrease of pituitary function, even in progressive cases of deterioration due to compression of the chiasm. Strict monitoring of the vision and a control MRI is obligatory to evaluate the treatment after 48-36 h. Tissue diagnosis is mandatory when there are multiple relapses. We present a case of progressive visual deterioration in hypophysitis, successfully treated with high-pulse dose prednisolone.


The statement has described the clinical features of this syndrome. It is usually a late complication (the patient was operated 20 years ago for a Bilroth II, remember that it is a partial gastrectomy, closure of the gastric stump and anastomosis of the first jejunal loop to the stump), it is accompanied by postprandial pain, abdominal distension. What has occurred is a stenosis of the afferent loop, so that biliary and pancreatic secretions do not mix with the bolus, they accumulate, produce pain that is relieved by vomiting, fat absorption is not possible (lack of pancreatic lipase), so there is diarrhea, and if associated with bacterial overgrowth, there is malabsorption of vitamin B12. If it were gastric adenocarcinoma, they would have spoken of constitutional syndrome, extradigestive manifestations (sister Maria Jose node, Krukenberg tumor, Virchow node). It is not dumping because it does not speak of vegetative symptoms (palpitations, facial flushing, etc...). Biliary reflux gastropathy is an endoscopic diagnosis, moreover it is not associated with diarrhea or malabsorption.

The statement has described the clinical features of this syndrome. It is usually a late complication (the patient was operated 20 years ago for a Bilroth II, remember that it is a partial gastrectomy, closure of the gastric stump and anastomosis of the first jejunal loop to the stump), it is accompanied by postprandial pain, abdominal distension. What has occurred is a stenosis of the afferent loop, so that biliary and pancreatic secretions do not mix with the bolus, they accumulate, produce pain that is relieved by vomiting, fat absorption is not possible (lack of pancreatic lipase), so there is diarrhea, and if associated with bacterial overgrowth, there is malabsorption of vitamin B12. If it were gastric adenocarcinoma, they would have spoken of constitutional syndrome, extradigestive manifestations (sister Maria Jose node, Krukenberg tumor, Virchow node). [HIDDEN] because it does not speak of vegetative symptoms (palpitations, facial flushing, etc...). Biliary reflux gastropathy is an endoscopic diagnosis, moreover it is not associated with diarrhea or malabsorption.

Point out from among the following the most likely complication presented by a patient operated, 20 years ago, of gastric ulcer by antrectomy and gastrojejunostomy (Billroth II) who comes to your office referring postpradial abdominal pain, abdominal distension, diarrhea and analytical data of malabsorption of fats and vitamin B12:

Rapid gastric emptying syndrome (dumping).

Afferent loop syndrome with bacterial overgrowth.

InternalMed_Harrison

afferent loop synDromes Although rarely seen today as a result of the decrease in the performance of Billroth II anastomosis, two types of afferent loop syndrome can occur in patients who have undergone this type of partial gastric resection. The more common of the two is bacterial overgrowth in the afferent limb secondary to stasis. Patients may experience postprandial abdominal pain, bloating, and diarrhea with concomitant malabsorption of fats and vitamin B12. Cases refractory to antibiotics may require surgical revision of the loop. The less common afferent loop syndrome can present with severe abdominal pain and bloating that occur 20–60 min after meals. Pain is often followed by nausea and vomiting of bile-containing material. The pain and bloating may improve after emesis. The cause of this clinical picture is theorized to be incomplete drainage of bile and pancreatic secretions from an afferent loop that is partially obstructed. Cases refractory to dietary measures may need

[The Soupault-Bucaillle operation in the treatment of Billroth II gastric resection syndrome].

The study analyzes the benefits related to the gastroduodenojejunoplasty (GDJP) according to Soupault & Bucaille, adopted as the corrective treatment of the Billroth II gastric resection syndrome in those cases resistant to the dieting-pharmacological supports. Our experience is based on 18 cases (13 males, 5 females, mean age 39 yrs), treated from 1982 to 1987 with GDJP for a gastric resection syndrome. The patients were observed 5 years after their resection: 10 presented with an atrophic gastritis/gastric atrophy and all had a diffuse acute phlogosis in presence of biliary storage. Manual anastomoses were performed in the first 8 cases, while staplers were used in the remaining cases. Results were quite satisfying; no operative mortality or specific complications, nor pain and biliary vomiting were registered; 14 patients over 18 (77%) gained weight significantly; only 1 patient reported low-intense early "dumping-like" symptoms easily controlled by medical therapy. Endoscopy showed no biliary reflux in all cases. Biopsies of the stump, carried on before and after the GDJP intervention, showed a marked reduction of the inflammatory aspects in 76% (13) of the patients. Among the 10 patients with atrophic gastritis/gastric atrophy, only 2 (20%) presented a significant increase in the number of gastric parietal cells and gastric principal cells.

[Restoration of duodenal transit in the surgical treatment of postgastrectomy syndrome. The Soupault-Bucaille procedure].

Between 5-50% of patients undergoing gastric resection still develop postgastrectomy syndrome in spite of the development of surgical techniques and an improved knowledge of gastrointestinal physiopathology: unfortunately, 2-5% of these patients require surgery. The technique to be used depends on a careful clinical and instrumental evaluation aimed at identifying the dominant type of postresection syndrome and any associated lesions, on the previous operation and obviously on the intraoperative situation. Soupault-Bucaille's gastroduodenojejunoplasty aims to correct the postresection syndrome by reinserting the duodenum in the digestive circuit, interposing between it and the gastric stump a jejunal loop made from the efferent (or afferent in the case of Billroth II with efferent on the lesser gastric curvature). This reconstitutes a paraphysiological condition of the digestive circuit, reduces biliary reflux and resolves acute gastritis. It is indicated in patients affected by early or late dumping syndrome, or multi-deficiency syndromes that do not respond to pharmacological therapy. The presence of concomitant biliary reflux is not a contraindication for this procedure, but confirms the need. Roux-en-Y is able to produce better results in postgastrectomy syndromes with alkaline gastritis and/or esophagitis sustained by biliary reflux, gastric atonia and afferent loop syndromes.

[Gastrocolic fistula - a rare cause of cachexia and polyneuropathy].

Gastrocolic fistula is a rare clinical disorder which in the past most often occurred after gastric surgery or carcinoma of the gastrointestinal tract. However, during the last decade an increasing number of cases after benign gastric ulcers have been described. Most common symptoms have been weight loss, abdominal pain, diarrhea and copremesis. A 49-year-old cachectic patient presented with a 2-year history of abdominal discomfort and diarrhea. He reported a weight loss of 32 kg during this period and was finally unable to move because of exhaustion. Furthermore, he suffered of burning paresthesia of the legs and the abdomen. His medical history included a Billroth II operation because of recurrent ulcer disease in 1987. Barium enema revealed a gastrocolic fistula which caused small bowel bacterial overgrowth with villous atrophy and malabsorption and development of polyneuropathy. The fistula was surgically resected, and postoperatively, the patient improved and regained his weight. Gastrocolic fistula is a rare cause of diarrhea and should be considered in clinical practice. Barium enema is superior to endoscopy in detecting gastrocolic fistula.

Postgastrectomy syndromes.

The preceding briefly summarizes some mechanical, metabolic, and motility disturbances that develop after gastric operations. Clearly, the more thorough the search and questions, the greater the incidence of minor, moderate, or severe impairment by one or more of these disorders. Our previous fears in treating benign ulcer disease were, first, mortality and, then, recurrent ulcers. Postgastrectomy syndromes were thought of secondarily. The seriousness, frequency, and lack of specific treatment available for most postgastrectomy syndromes were generally not recognized. While serious sequelae are infrequent, some take years to develop. A few, such as cancer, are regrettable even if treatable. Surgical correction of most of these syndromes is at best 50 to 80 percent effective. Poor selection of patients, mixed symptoms, and our inability to repiece vagus nerves and excised antrums make it difficult, if not impossible, to correct totally the anatomic and physiologic changes. Surgical intervention is infrequent. For some abnormalities, such as bile reflux gastritis, correction is uniformly good if gastric emptying is satisfactory and the syndrome exists alone. For others, such as dumping and diarrhea, treatment is less exacting, and the variety of operative alternatives often confuses rather than helps. My own continually changing experiences have taught me to correct the major disability in the simplest way. My experience with take-down of gastrojejunostomies and pyloroplasties is limited but encouraging. My satisfaction with Roux-en-Y conversions of Billroth II resections in reflux gastritis has been extended to the correction of diarrhea and dumping. Creating a long isoperistaltic limb between stomach and jejunum has provided surprisingly excellent relief for the problems of rapid emptying, although I have not objectively verified emptying changes in all successfully treated patients. The best results come with avoidance of these disorders. It is hoped that simpler operations for ulcer disease will continue to gain in popularity. Highly selective vagotomy is an easier, more attractive alternative than any of the aforementioned remedial procedures, particularly if the long-term results are good.

Causes of malabsorption in the elderly.

The pathogenesis of malabsorption has been studied in 70 patients who presented over the age of 65 years and who were referred to a special investigative unit. Often more than one cause was apparent. Fourteen patients had pancreatic insufficiency, most of whom had no history of pain, alcoholism or gallstones. Twenty-three patients had the postgastrectomy syndrome or small-bowel diverticulosis or both. There were eight coeliacs aged 65-72 years at diagnosis. Fifteen patients had an anatomically normal small bowel; eight of these were over 80 years old, and 10 had vitamin B12 deficiency of whom five had confirmed pernicious anaemia. Enterobacterial overgrowth was a feature of all diagnostic groups except pancreatic and coeliac disease. Vitamin B12 deficiency may be an effect of malabsorption, but can also be a cause through impairment of enterocyte function. The association of pernicious anaemia and B12 deficiency with otherwise unexplained malabsorption and bacterial overgrowth suggests that gastric atrophy is a major causal factor in this syndrome, combined in some cases with a 'vicious circle' of B12 malabsorption and deficiency.

[Late follow-up of gastrectomized patients for peptic ulcer: clinical, endoscopic and histopathological aspects].

The gastrectomy is an uncommon procedure because the proton bomb inhibitors associated to the antibiotic outlines used to eradicate the Helicobacter pylori changed the focus of the peptic ulcer treatment. Later evaluation on those patients who underwent partial gastrectomy as a treatment for peptic ulcer, at that time when any drug to eradicate the Helicobacter pylori was not used. The clinical evaluation included the late postoperative symptoms and postgastrectomy syndromes like dumping, diarrhea, alkaline gastritis and nutritional aspects. The upper digestive endoscopy analysed the surgery reconstruction and the gastric stump, the duodenum and the jejunum mucosa aspects. The histopathological evaluation included looking for Helicobacter pylori by using two different methods: histology and urease test. Fifty-nine patients, 44 (74.6%) male, median age 55.5 years old (range from 31 to 77 years old), who underwent a clinical interview and an upper digestive endoscopy. Paraffin blocks from the surgical specimen were reviewed in order to find out if the patients did have or did not have Helicobacter pylori before surgery. The final results show that most of the patients had very good and good clinical evolution (Visick I e II) in 96%. The most common symptoms on late postoperative are mild dyspepsia with or without Helicobacter pylori, and diarrhea, anemia and dumping occurred in, respectively, 11 (18.6%), 2 (3.4%) and 2 (3.4%) cases. The Billroth I reconstruction had the best clinical results on statistical rate. The endoscopic finding showed normal results in the most number of cases, and reflux alkaline gastritis or erosive gastritis in a few cases. Ulcer recurrences were diagnosed in two patients (3.4%), and both had positive Helicobacter pylori. Most of the patients had Helicobacter pylori (86%) before surgery and also in the postoperative time (89.9%). The patients had a very good clinical evolution after the gastrectomy. The Billroth I reconstruction had the best clinical results. The Helicobacter pylori is still present on gastric stump in late postoperative time, and we believe that it does not bring any negative influence to surgical results.

Metabolic problems after gastric surgery.

The findings on dumping syndrome (DS) are not consistent considering its relations with age, sex, weight/height, smoking habits, race, dose of oral glucose, the time elapsed since surgery, the function of exocrine pancreas nor the duration of ulcer symptoms. The patients after total gastrectomy (TG) may present relative postprandial lack of insulin. As a sign of long-term hyperglycemia elevated HbA1 has been measured in DS patients. Oral galactose test may reveal new features of DS. Abnormalities in splanchnic blood circulation as well as release of intestinal hormones are involved with DS. Dietary habits including fibers, pectin and guar gum, play a central role in the prevention and treatment of DS. In unresponsive cases several operative methods have been applied with success. Alkaline reflux gastritis is most often seen after B II and I reconstructions and after pyloroplasty. Chronic diarrhea follows mostly after truncal vagotomy. Ten to 50% of patients after gastrectomy (GE) waste 10 to 20% of their body weight because of decreased food, energy, vitamin and mineral intake caused by eating-related symptoms. Vitamin and mineral supplements, a small snack 20 min before the major meal, digestive enzymes, treatment of colonization with antibiotics and protein foods may help. About 50% of GE patients show iron deficiency anemia. Easily dissolved iron between meals with ascorbic acid give the most effective response. Deficiency of vitamin B12 or of folate may develop as megaloblastic anemia. B12 supplement and antibiotics are effective in bacterial overgrowth, but surgical correction is necessary in troublesome blind loop. Folic acid deficiency is corrected by oral folic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Short bowel syndrome

The resection of specific areas of the small bowel can lead to distinct symptoms in short bowel syndrome. The resection of the ileum leads to a malabsorption of vitamin B12, bile acids and the fat soluble vitamins A, D, E and K. Loss of the distal ileum also leads to loss of inhibitory hormones; leading to gastric hypersecretion, intestinal hypermotility (decreases in the intestinal transit time) leading to secretory diarrhea and macronutrient, micronutrient, vitamin and mineral deficiencies. Loss of the ileocecal valve leads to small intestinal bacterial overgrowth(SIBO) as bacterial flora normally found in the large intestines migrate proximally and colonize the small intestines leading to further malabsorption. SIBO leads to malabsorption as the bacteria colonizing the small intestine metabolize nutrients, directly competing with the intestinal absorption of nutrients. The bacteria colonizing the small intestines in SIBO may also cause bile acid deconjugation leading to

[The reinsertion of the duodenum into the digestive circuit. The indications and surgical technics in operated stomach syndromes].

The authors analyse, retrospectively, the experience of the Clinic of Surgery III. Cluj-Napoca, in the indications and surgical methods for reintroducing the duodenum in the digestive circuit in the syndromes of the stomach operated for benign affections. Between 1974 and 1987, the duodenum was reinstated in the digestive circuit in 37 patients, operated previously for duodenal ulcer (32 cases), gastric ulcer (3 cases), syndrome of mesenteric clip (2 cases). The primary surgeries that led to the exclusions of the duodenum from the digestive tract were gastroenteroanastomosis in 4 cases, and the gastric resections with gastrojejunal anastomoses of the Billroth II type in 33 cases (Reichel-Polya in 28 cases. Hoffmeister-Finsterer in 3 cases, Roux in 2 cases). The reintroduction of the duodenum in the digestive circuit, based on clinical and paraclinical criteria, was indicated in anastomotic ulcer (in 17 cases), gastric ulcer following gastroenteroanastomoses (in 1 case), syndrome of afferent loop (in 11 cases), persistent "dumping" syndrome (in 8 cases), association of plurideficiency syndrome (in 54% of the cases). The way of reconstructing the duodenum was adapted to the type and correctness of the primary operation, to the dominant clinical syndrome and associated lesions to the biological background and possibilities offered by the intrasurgical situation: reconversion by direct gastroduodenal anastomosis after degastrogastrectomy was used in 31 cases, the indirect methods by transposition of the afferent loop (Soupault--Bucaille) in 4 cases, or of the afferent one (Henley)--1 case gastrography and segmentary enterectomy in 1 case. The postoperative complications appeared in 35.1% of case, with a mortality of 8.1%. The therapeutic results were good and very good in 89.3% of the cases. The authors insist on the importance of maintaining the duodenum in the digestive circuit, during the primary surgeries for preventing some severe postsurgical syndromes.

Vitamin B12 deficiency

Impaired absorption of vitamin B12 leads to pernicious anemia a type of megaloblastic anemia. Pernicious anemia comes about from the lack of gastric intrinsic factor produced by parietal cells in the stomach, and needed in the ileum for the absorption of vitamin B12. Pernicious anemia is the most common cause of vitamin B12 deficiency. Any disruption that leads to the loss of parietal cells can lead to malabsorption, and includes atrophic gastritis, a condition that often affects the elderly, and gastric surgeries that involve the removal of all or part of the stomach, such as Roux-en-Y gastric bypass surgery. Surgical removal of the small bowel such as in Crohn's disease results in short bowel syndrome and the inability to absorb vitamin B12. Impaired absorption can also result from blind loop syndrome where an overpopulation of bacteria in the small intestine absorb the vitamin. Some infections such as giardiasis, and diphyllobothriasis caused by parasites can also cause

Highly selective vagotomy and gastrojejunostomy in the treatment of peptic ulcer induced gastric outlet obstruction.

The incidence of peptic ulcer-induced gastric outlet obstruction is constantly declining. The aim of this study was to present our results in the treatment of gastric outlet obstruction with highly selective vagotomy and gastrojejunostomy. This retrospective clinical study included 13 patients with peptic ulcer-induced gastric outlet obstruction operated with higly selective vagotomy and gastrojejunostomy. A 3-year follow-up was conducted including clinical interview and upper gastrointestinal endoscopy on 1 and 3 years after the surgery. The most common preoperative symptom was vomiting (in 92.3% of patients). The mean preoperative body mass index was 16.3 +/- 3.1 kg/m2, with 9 patients classified preoperatively as underweight. There were no intraoperative complications, nor mortality. At a 3-year follow-up there was no ulcer recurrence. Delayed gastric emptying was present in 1, bile reflux in 2, and erosive gastritis in 1 patient. Two patients suffered from mild "dumping" syndrome. Higly selective vagotomy combined with gastrojejunostomy is a safe and easily feasible surgical solution of gastric outlet obstruction induced by peptic ulcer. Good functional results and low rate of complications can be expected at a long-term follow-up.

Gastrectomy

Another side effect is the loss of ghrelin production, which has been shown to be compensated after a while. Lastly, this procedure is post-operatively associated with decreased bone density and higher incidence of bone fractures. This may be due to the importance of gastric acid in calcium absorption. Post-operatively, up to 70% of patients undergoing total gastrectomy develop complications such as dumping syndrome and reflux esophagitis. A meta-analysis of 25 studies found that construction of a "pouch", which serves as a "stomach substitute", reduced the incidence of dumping syndrome and reflux esophagitis by 73% and 63% respectively, and led to improvements in quality-of-life, nutritional outcomes, and body mass index. After Bilroth II surgery, a small amount of residual gastric tissue may remain in the duodenum. The alkaline environment causes the retained gastric tissue to produce acid, which may result in ulcers in a rare complication known as retained antrum syndrome.

Partial gastrectomy for peptic ulcer by the Krønlein method. An outpatient follow-up study 12 years later with particular reference to endoscopy with biopsy and brush cytology and to clinical-chemical and radiological results.

Forty-six patients were studied 12 years after partial gastrectomy for peptic ulcer. They had all been subjected to a standard Billroth II type operation as described by Krønlein, with emphasis laid upon the transverse position of the gastrojejunostomy. The clinical examination was supplemented by an outpatient gastroscopy with photography, biopsy and brush cytology, and by a series of blood analyses and X-ray of the gastric remnant. The general finding on gastroscopy was a slightly injected mucosa with flattened folds near the anastomosis, no or slight reflux of bile. The cytological examination revealed metaplasia in 7.5-15 per cent of the specimens, no sign of dysplasia or carcinoma. Biopsy showed severe atrophic gastritis in 0-13 per cent of the specimens, slight to moderate in 58-96 per cent, no signs of cellular atypia or irregular arrangements. Judged by the results of blood analyses a deficiency in iron, Vitamin B12 or both, was demonstrated in about 25 per cent of patients and of these more than 50 per cent were anaemic. X-ray examination showed that 70 per cent of the patients had an emptying time of the gastric remnant of 10-20 minutes. A transverse position of the anastomosis could be demonstrated in about 67 per cent. The necessity of a close follow-up of these patients is stressed.

Achlorhydria -- Complications

The majority of the complications found in achlorhydria are due to nutrient deficiency. They are also more common compared to the other complications. Iron deficiency Vitamin-B12 deficiency Vitamin-D and calcium deficiency leading to osteoporosis and bone fracture Gastric adenocarcinoma Gastric carcinoid tumor Small intestinal bacterial overgrowth syndrome

Gastroparesis

Diagnosis is via one or more of the following: barium swallow X-ray, barium beefsteak meal, radioisotope gastric-emptying scan, gastric manometry, and esophagogastroduodenoscopy (EGD). Complications include malnutrition, fatigue, weight loss, vitamin deficiencies, intestinal obstruction due to bezoars, and small intestine bacterial overgrowth. Treatment includes dietary modifications, medications to stimulate gastric emptying, medications to reduce vomiting, and surgical approaches. Signs and symptoms The most common symptoms of gastroparesis are the following: Chronic nausea Vomiting (especially of undigested food) Abdominal pain A feeling of fullness after eating just a few bites

Postgastrectomy syndromes.

Anatomic and physiological changes introduced by gastric surgery result in postgastrectomy syndromes in approximately 20% of patients. Most of these disorders are caused by operation-induced abnormalities in the motor functions of the stomach, including disturbances in the gastric reservoir function, the mechanical-digestive function, and the transporting function. Division of the vagal innervation to the stomach and ablation or bypass of the pylorus are the most significant factors contributing to postgastrectomy syndromes. Either rapid or slow emptying may result, depending on the relative importance of lack of a compliant gastric reservoir, loss of an effective contractile force, and loss of controlling factors that slow or speed gastric emptying and result in duodenal-gastric reflux. Clearly defining which syndrome is present in a given patient is critical to developing a rational treatment plan. In syndromes with slow gastric emptying, bilious vomiting, or alkaline reflux gastritis, the use of endoscopy is essential to rule out mechanical causes of the syndrome. Contrast radiography and scintigraphic gastric emptying studies are useful to document rapid or delayed gastric emptying. Postgastrectomy syndromes often abate with time. Conservative measures, including medical, dietary, and behavioral therapy, should be given at least a 1-year trial. If these nonoperative measures fail, surgical therapy is recommended. The Roux-en-Y gastrojejunostomy is useful for patients with dumping, because it slows gastric emptying and the transit of chyme through the Roux limb. The same operation helps patients with alkaline reflux gastritis, because it diverts pancreaticobiliary secretions away from the gastric remnant. Near-total gastrectomy, which reduces the size of a flaccid gastric reservoir, can be used to treat delayed gastric emptying. This operation should be combined with the Roux procedure to prevent postoperative reflux gastritis and esophagitis. Newer techniques, such as gastrointestinal pacing and the uncut Roux operation, may improve the treatment of the postgastrectomy syndromes in the future.

A porspective study of parietal cell vagotomy and selective vagotomy-antrectomy for treatment of duodenal ulcer.

A prospective, randomized, study involving 92 patients who required elective operation for treatment of duodenal ulcer was performed to compare the results of Parietal Cell Vagotomy (PCV) and selective vagotomy-antrectomy Billroth I (SV-A-BI). The protocol was broken twice. One patient was unable to undergo PCV because of pyloric stenosis and one patients underwent Billroth II anastomosis instead of Billroth I because of post-bulbar stenosis. Performance of PCV was never aborted because a patient was obese. There were no deaths. Diarrhea, dumping and other gastric complaints were less frequent after PCV than after SV-A-BI for all time periods studies up to two years. Two months after operation, the Hollander tests were negative in 59% of patients after PCV and in 100% after SV-ABI. Inhibition of Bao and MAO were also significantly less after PCV than after SV-A-BI. Since vagotomy of the parietal cell mass was identical in both groups of patients it was concluded that the differences in the secretory rates and the fewer negative Hollander tests in the PCV group than in the SV-A-BI group were due to retention of the antrum irrespective of its innervation. There was no explanation for the gradual increase in the BAO in the PCV group. One recurrent ulcer occurred in the PCV group in a patient who overindulged in alcohol and aspirin. After 4 days of medical management, this superficial ulcer healed as demonstrated by endoscopy. There were no recurrent ulcers after SV-A-BI. As a result of this study, it is concluded that PCV is superior to SV-A-BI because of the lower frequency of postoperative complications, diarrhea, dumping and other symptoms associated with gastric surgery. PCV may be the operation of choice for the elective treatment of duodenal ulcer; however, it remains undetermined whether the recurrent ulcer rate following PCV will be sufficiently low that the procedure can retain a position of superiority over SV-A-BI.

List of MeSH codes (C06)

– peptic ulcer – duodenal ulcer – esophagitis, peptic – peptic ulcer perforation – stomach ulcer – zollinger-ellison syndrome – stomach diseases – achlorhydria – diverticulosis, stomach – duodenogastric reflux – bile reflux – gastric antral vascular ectasia – gastric dilatation – gastric outlet obstruction – pyloric stenosis – pyloric stenosis, hypertrophic – gastritis – gastritis, atrophic – gastritis, hypertrophic – gastroparesis – peptic ulcer – peptic ulcer perforation – stomach ulcer – postgastrectomy syndromes – dumping syndrome – stomach neoplasms – stomach rupture – stomach volvulus – zollinger-ellison syndrome – tuberculosis, gastrointestinal – visceral prolapse – liver diseases – cholestasis, intrahepatic – alagille syndrome – liver cirrhosis, biliary – fatty liver – fatty liver, alcoholic – reye syndrome – focal nodular hyperplasia

[Peptic ulcer: late complications of the surgical treatment].

The incidence of surgical treatment of peptic ulcer decreased in the last two decades. The majority of procedures for surgical management of peptic disease impairs the ability of the stomach to receive and to store food. The intake of high protein-caloric content diets can improve some nutritional deficits expressed by loss of body weight and anemia. The mechanism responsible for diarrhea is unknown, but truncal vagotomy has the highest incidence. It is usually episodic, lessens over the first year after operation and rarely remains a severe problem. The decreasing levels of colecistokinin response after meal in gastrectomy and the division of hepatic branch of anterior vagus can cause gallbladder sludge and stone formation. Alkaline reflux explains gastritis and esophagitis after partial gastric resection. Surgical duodenal diversion, like a Roux-en-Y limb, have been successful in its control. The mechanism that leads to the dumping syndrome are loss of gastric reservoir function and rapid emptying of hyperosmolar meals into small intestine. Somatostatin analogues improve the symptoms caused by abnormal release of neurohormonal agents responsible of the behaviour of the gastrointestinal tract after meals. Cancer of gastric remanent may be due to increased bacterial overgrowth and nitrosation formation. The endoscopic follow-up is essential for early diagnosis of the stump cancer. In spite of all complications, the surgeon cannot have hesitations by carrying out radical approach meanly during catastrophic emergencies of peptic disease i.e. in elderly aged patients. Nowadays, the control of chronic sequelas is easy with conservative therapeutic.

Alkaline reflux gastritis.

Alkaline reflux gastritis and the symptoms associated with alkaline reflux gastritis have been reported in the medical literature since shortly after Billroth successfully performed his first gastrectomy in the 1880s. The disease process is produced by, or at least is associated with, the reflux of alkaline secretions into the gastric remnant. Although it occurs after any procedure that ablates the pylorus including pyloroplasty, it would appear to be most common after a Billroth II gastrojejunostomy. How the alkaline secretions cause the gastritis is still controversial. Clearly, the most effective therapy is to reroute the secretions from the biliary tract, pancreas, and duodenum so that they will not reflux into the gastric remnant. This is most effectively accomplished by a Roux-en-Y gastrojejunostomy with the afferent limb measuring at least 18 inches (40 cm). The surgeon and the patient should be aware that the construction of such a gastric outlet channel is associated with delayed gastric emptying. The etiology of this impaired emptying is also controversial. If the patient has symptoms of dumping (either early or late), these symptoms may also be abated using the Roux limb. At least 40% of patients will have gastric outlet obstruction. Supportive therapy is appropriate in the majority of these patients.

InternalMed_Harrison

malDiGestion anD malabsorption Weight loss can be observed in up to 60% of patients after partial gastric resection. Patients can experience a 10% loss of body weight, which stabilizes 3 months postoperatively. A significant component of this weight reduction is due to decreased oral intake. However, mild steatorrhea can also develop. Reasons for maldigestion/malabsorption include decreased gastric acid production, rapid gastric emptying, decreased food dispersion in the stomach, reduced luminal bile concentration, reduced pancreatic secretory response to feeding, and rapid intestinal transit. Decreased serum vitamin B12 levels can be observed after partial gastrectomy. This is usually not due to deficiency of IF, since a minimal amount of parietal cells (source of IF) are removed during antrectomy. Reduced vitamin B12 may be due to competition for the vitamin by bacterial overgrowth or inability to split the vitamin from its protein-bound source due to hypochlorhydria.

Gastric bypass surgery

Mini-gastric bypass (MGB) The mini-gastric bypass procedure was first developed by Robert Rutledge from the US in 1997, as a modification of the standard Billroth II procedure. A mini gastric bypass creates a long narrow tube of the stomach along its right border (the lesser curvature). A loop of the small gut is brought up and hooked to this tube at about 180 cm from the start of the intestine. Numerous studies show that the loop reconstruction (Billroth II gastrojejunostomy) works more safely when placed low on the stomach, but can be a disaster when placed adjacent to the esophagus. Today thousands of "loops" are used for surgical procedures to treat gastric problems such as ulcers, stomach cancer, and injury to the stomach. The mini-gastric bypass uses the low set loop reconstruction and thus has rare chances of bile reflux.

Adjustable gastric band

Unlike more open forms of weight loss surgery (e.g. Roux-en-Y gastric bypass surgery (RNY), Biliopancreatic diversion (BPD) and Duodenal Switch (DS)), gastric banding does not require cutting or removing any part of the digestive system. It is removable, requiring only a laparoscopic procedure to remove the band, after which the stomach usually returns to its normal pre-banded size so it is not unusual for a person to gain weight after having a band removed. However, it is not entirely reversible as adhesions and tissue scarring are inevitable. Unlike those who have procedures such as RNY, DS, or BPD, it is unusual for gastric band patients to experience any nutritional deficiencies or malabsorption of micro-nutrients. Calcium supplements and Vitamin B12 injections are not routinely required following gastric banding (as is often the case with RNY, for example). Gastric dumping syndrome issues also do not occur since intestines are not removed or re-routed.

Gastric Resection -- Complications -- Late Complications

Bile reflux gastritis Dumping syndrome Afferent and efferent limb syndrome Malnutrition and nutritional deficiencies Internal hernia or Peterson hernia Anastomotic stricture Marginal ulcer Cancer recurrence

Retained antrum syndrome

Retained antrum syndrome or retained gastric antrum syndrome is one of the rare postgastrectomy syndromes. It happens after Billroth II surgery and the mechanism involved is the inadequate removal of the distal antrum and pylorus during resection of the antrum and gastrojejunostomy. Lack of the usual acid-secreting gastric glands makes the antral segment continually exposed to the alkaline environment of the duodenum, which causes it to secrete excessive acid and be prone to form ulcers. References Gastrointestinal tract disorders

Surgery_Schwartz

operation successfully in the management of the dumping syndrome. Although this is probably the procedure of choice in the small group of patients requiring operation for severe dumping fol-lowing gastric resection, gastric stasis may result, particularly if a large gastric remnant is left. In the presence of significant gastric acid secretion, marginal ulceration is common after both jejunal interposition and Roux-en-Y procedures; thus, concomitant vagotomy and hemigastrectomy should be con-sidered. The theoretical possibility of treating postpyloroplasty dumping with a Roux-en-Y to the proximal duodenum (the duodenal switch, a potentially reversible operation) has not yet been reported (Fig. 26-67). Because pyloric ablation seems to be the dominant factor in the etiology of dumping, it is not sur-prising that conversion of Billroth II to Billroth I anastomosis has not been successful in the treatment of dumping.DiarrheaDiarrhea following gastric surgery may be the result of trun-cal

An Unusual Presentation of Obstructive Jaundice Due to Dilated Proximal Small Bowel Loops After Gastrojejunostomy: Afferent Loop Syndrome.

Afferent loop syndrome is reported to be one of the very rare complications after gastrojejunostomy. The usual presentation in patients is with abdominal pain, distension and vomiting. It may present acutely because of complete obstruction, usually occurs early after surgery and is lethal in its course unless treated promptly with surgical management. In chronic cases obstruction is intermittent. There may be a reflux of bowel material into the biliary system and because of bacterial overgrowth patient may present with ascending cholangitis and obstructive jaundice. Here we report a case of 43-year-old gentleman presenting with jaundice, diffuse abdominal pain and distension. Later on, he was found to have a recurrence of gastric carcinoma associated with peritoneal carcinomatosis after subtotal gastrectomy and gastrojejunostomy for gastric carcinoma one year ago. He was diagnosed to be a case of afferent loop syndrome presenting as obstructive jaundice. The patient was managed conservatively by endoscopic decompression after confirmation of the diagnosis of afferent loop syndrome.

Alkaline reflux gastritis.

Any surgical procedure that ablates the pyloric sphincter mechanism permits increased reflux of duodenal fluid into the stomach or gastric remnant. Although it is reported as most common with Billroth II gastrectomy, our experience indicates that reflux is nearly as frequent after Billroth I gastroduodenostomy and is not at all infrequent after pyloroplasty. The precise constituents of duodenal fluid which damage the gastric mucosa remain controversial. The best present evidence is that the bile acids are probably essential, but that one or more other constituents of duodenal content are also necessary. The clinical history differs significantly from chronic afferent loop syndrome in that the quality of pain is different, pain tends to be more continuous and less closely related to food-taking, and bile vomiting does not provide dramatic relief, often containing food due to coexistent interference with gastric emptying. Diagnosis is confirmed by gross endoscopic findings and characteristic histopathologic changes in the endoscopic biopsies. Treatment with an interposed isoperistaltic jejunal segment has been disappointing. Only four of ten patients experienced lasting relief, indicating that the relatively short 10 to 12 cm. of jejunum does not adequately prevent duodenogastric reflux. We have, therefore, shifted to the Roux-en-Y duodenal diversion implanting the afferent limb 40 cm. caudad to the gastrojejunostomy. Results have been excellent in 24 of 25 cases with prompt improvement in gastric emptying, absence of bile vomiting, progressive regression in abdominal distress and progressive improvement in nutrition. Endoscopic evaluation at three to four months has indicated marked gross improvement and striking histologic improvement in 23 of 25 cases. The question is raised whether the Roux-en-Y reconstruction should not be used primarily, particularly if both vagotomy and antrectomy are to be performed for peptic ulcer. Both the afferent loop syndrome and alkaline reflux gastritis would be prevented, and it is doubted that the incidence of marginal ulcer would increase appreciably.

Bloating

Common causes of abdominal bloating are: Overeating Gastric distension Lactose intolerance, fructose intolerance and other food intolerances Premenstrual Syndrome Food allergy Aerophagia (air swallowing, a nervous habit) Irritable bowel syndrome Celiac disease Non-celiac gluten sensitivity Partial bowel obstruction Gastric dumping syndrome or rapid gastric emptying Gas-producing foods Constipation Visceral fat Splenic-flexure syndrome Menstruation, dysmenorrhea Polycystic ovary syndrome and ovarian cysts Alvarez' syndrome, bloating of unknown or psychogenic origin without excess gas in the digestive tract Massive infestation with intestinal parasites (e.g., Ascaris lumbricoides) Diverticulosis Certain medications, such as phentermine Occurs in some due to salivary hypersecretion and dehydration. Ovarian cancer Important but uncommon causes of abdominal bloating include:

Small bowel bacterial overgrowth in symptomatic older people: can it be diagnosed earlier?

In older people, small bowel bacterial overgrowth syndrome may be a common, but under-diagnosed, cause of diarrhoea and nutrient malabsorption. We aim to determine which clinical features and baseline laboratory investigations indicate a high likelihood of small bowel bacterial overgrowth as defined by a positive glucose breath test. A retrospective analysis of records for all patients referred for glucose breath test over a 6-year period to a teaching hospital. Out of 197 referrals, 168 patient records were located and analysed (62 male, 106 female; median age 65). Patient characteristics predictive of a positive glucose breath test were: increasing age (p < 0.01), low serum vitamin B12 (p = 0.02), low serum albumin (p = 0.03), previous partial gastrectomy (p < 0.01), previous right hemi-colectomy (p < 0.01), presence of small bowel diverticulae (p = 0.01) and concurrent use of a proton pump inhibitor (p < 0.01). 52.5% (n = 21/40) of patients studied who were over 75 years old versus 21.8% (n = 28/128) of those under 75 years old had a positive glucose breath test (p < 0.01). The median time to diagnosis, from first hospital visit to positive glucose breath test, was 39 weeks. There is often a significant delay in diagnosis of small bowel bacterial overgrowth. We suggest that this diagnosis should be considered earlier in the investigative algorithm in older patients with indicative symptoms and a predisposing factor (including previous partial gastrectomy, previous right hemi-colectomy, small bowel diverticulae or use of a proton pump inhibitor) or concurring laboratory indices (low vitamin B12 or albumin).

Experience with vagotomy--antrectomy and Roux-en-Y gastrojejunostomy in surgical treatment of duodenal, gastric, and stomal ulcers.

Gastroduodenostomy (Billroth I) is our reconstruction of choice following gastric resection for gastroduodenal ulcer. Dissatisfaction with a Billroth II anastomosis has led us in recent years to employ a Roux-en-Y diversion in selected cases, particularly those in which the pathologic state of the pyloroduodenal canal would render a Billroth I anastomosis unsafe. During the past 7 years, truncal vagotomy-antrectomy and Roux-en-Y (VARY) has been carried out in 50 selected patients: duodenal ulcer (DU) 13 patients, gastric ulcer (GU) 11 patients, and stomal ulcer (SU) 26 patients. Fourteen patients (28%) developed postoperative complications, of which nine (18%) were of major degree and five (10%) of a lesser degree. No hospital death occurred among the 50 patients. Five patients (10%) developed postoperative delayed gastric emptying and two of the five required revision of the Roux. Forty-five patients had no clinical problems with delayed emptying. Overall results showed a Visick grading of I in 72%, Visick II in 24%, and Visick III in 4%. Further analysis revealed that of the 13 patients with DU who had VARY, 62% were Visick I, 30% Visick II, and 8% Visick III. The 11 GU patients with VARY were graded Visick I 73% and Visick II 27%. Of 26 patients with SU who underwent VARY, 77% were Visick I, 19% Visick II, and 4% Visick III. Mild to moderate dumping took place in 8% of the 50 patients, mild diarrhea 10%, weight loss 10%, and no patient experienced alkaline reflux gastritis. Long-range postoperative gastric emptying studies among nine patients using a radionuclide revealed varying patterns of emptying. Overall clinical results have been satisfactory and we are continuing to use VARY in selected cases, particularly those in which a Billroth I reconstruction appears contraindicated.