A syndrome of acute non-cardiogenic pulmonary edema associated with hunting is prevalent in the drever breed, but etiology of this syndrome is currently unknown. Alveolar surfactant has a critical role in preventing alveolar collapse and edema formation. The aim of this study was to investigate, whether the predisposition to hunting associated pulmonary edema in drever dogs is associated with impaired biophysical properties of alveolar surfactant. Seven privately owned drever dogs with recurrent hunting associated pulmonary edema and seven healthy control dogs of other breeds were included in the study. All affected dogs underwent thorough clinical examinations including echocardiography, laryngeal evaluation, bronchoscopy, and bronchoalveolar lavage (BAL) as well as head, neck and thoracic computed tomography imaging to rule out other cardiorespiratory diseases potentially causing the clinical signs. Alveolar surfactant was isolated from frozen, cell-free supernatants of BAL fluid and biophysical analysis of the samples was completed using a constrained sessile drop surfactometer. Statistical comparisons over consecutive compression expansion cycles were performed using repeated measures ANOVA and comparisons of single values between groups were analyzed using T-test.

There were no significant differences between groups in any of the biophysical outcomes of surfactant analysis. The critical function of surfactant, reducing the surface tension to low values upon compression, was similar between healthy dogs and affected drevers.

The etiology of hunting associated pulmonary edema in drever dogs is not due to an underlying surfactant dysfunction.

Phaeochromocytomas and paragangliomas (PPGLs) release catecholamines leading to catecholamine-induced hypertensive (CIH) crises, with blood pressure greater than or equal to 180/120 mm Hg. CIH crises can be complicated by tachyarrhythmias, hypotension, or life-threatening target organ damage while treatment remains undefined, often requiring co-management between endocrinologists and cardiologists. Furthermore, biochemical diagnosis of a PPGL as a cause of a CIH crisis can be difficult to identify or confounded by comorbid conditions, potentially resulting in misdiagnosis. Here, we combine relevant evidence, 60 years of collective clinical experience, insights derived from assessing over 2600 patients with PPGL, and supplementary outcomes from 100 patients (treated at the National Institutes of Health) with a CIH crisis to inform diagnosis and treatment of CIH crises. Recognising that disparities exist between availability, cost, and familiarity of various agents, flexible approaches are delineated allowing for customisation, given institutional availability and provider preference. A CIH crisis and its complications are readily treatable with available drugs, with effective intervention defining an avenue for mitigating consequent morbidity and mortality in patients with PPGL.

Noncardiogenic pulmonary edema (NCPE) in hunting dogs is an uncommon and poorly described condition for which no preventive treatment is available. Two dogs were presented for recurrent respiratory distress strictly associated with hunting activities. Diagnosis was based on bilateral, symmetrical, interstitial-to-alveolar pattern in the caudodorsal lung fields on thoracic radiographs, exclusion of other causes, and spontaneous clinical and radiographic improvement. Considering that the pathogenesis of exercise-induced NCPE likely involves α- and β-adrenergic overstimulation, treatment with sympathetic blockers was used in both dogs. The first dog no longer showed respiratory signs during hunting activities. However, treatment failed to prevent respiratory distress in the other dog. Based on the large number of red blood cells in the bronchoalveolar lavage fluid of the second dog, exercise-induced pulmonary hemorrhage was suspected, as described in racing horses. The loop diuretic furosemide successfully prevented further hunting-associated respiratory distress episodes in this dog.

High-dose catecholamines can impair hypoxic pulmonary vasoconstriction and increase shunt fraction. We aimed to determine if Angiotensin II (Ang-2) is associated with improved PaO2/FiO2 and SpO2/FiO2 in patients in shock.

Adult patients at four tertiary care centers and one community hospital in the United States who received Ang-2 from July 2018-September 2020 were included in this retrospective, observational cohort study. PaO2, SpO2, and FiO2 were measured at 13 timepoints during the 48-h before and after Ang-2 initiation. Piecewise linear mixed models of PaO2/FiO2 and SpO2/FiO2 were created to evaluate hourly changes in oxygenation after Ang-2 initiation. The difference in the proportion of patients with PaO2/FiO2 ≤ 300 mm Hg at the time of Ang-2 initiation and 48 h after was also examined.

The study included 254 patients. In the 48 h prior to Ang-2 initiation, oxygenation was significantly declining (hourly PaO2/FiO2 change -4.7 mm Hg/hr, 95% CI - 6.0 to -3.5, p < .001; hourly SpO2/FiO2 change -3.1/hr, 95% CI-3.7 to -2.4, p < .001). Ang-2 treatment was associated with significant improvements in PaO2/FiO2 and SpO2/FiO2 in the 48-h after initiation (hourly PaO2/FiO2 change +1.5 mm Hg/hr, 95% CI 0.5-2.5, p  =  .003; hourly SpO2/FiO2 change +0.9/hr, 95% CI 0.5-1.2, p < .001). The difference in the hourly change in oxygenation before and after Ang-2 initiation was also significant (pinteraction < 0.001 for both PaO2/FiO2 and SpO2/FiO2). This improvement was associated with significantly fewer patients having a PaO2/FiO2 ≤ 300 mm Hg at 48 h compared to baseline (mean difference -14.9%, 95% CI -25.3% to -4.6%, p  =  .011). Subgroup analysis found that patients with either a baseline PaO2/FiO2 ≤ 300 mm Hg or a norepinephrine-equivalent dose requirement >0.2 µg/kg/min had the greatest associations with oxygenation improvement.

Ang-2 is associated with improved PaO2/FiO2 and SpO2/FiO2. The mechanisms for this improvement are not entirely clear but may be due to catecholamine-sparing effect or may also be related to improved ventilation-perfusion matching, intrapulmonary shunt, or oxygen delivery.

Pheochromocytoma most commonly presents with the triad of paroxysms of headache, palpitations, and diaphoresis. Pheochromocytoma crisis, caused by a supra-physiological surge of catecholamine release, is an endocrine emergency that can present with various clinical manifestations. Acute pulmonary edema is one of the manifestations of pheochromocytoma crisis and can be either cardiogenic or non-cardiogenic. Here, we report cases of acute pulmonary edema of each type, related to pheochromocytoma crisis, which were presented to our district general hospital in 2020.

Pheochromocytomas are rare endocrine tumors that can have a significant impact on a variety of organ systems, including the cardiovascular system. Although the pathophysiology is not completely understood, pheochromocytomas exert their effects through high levels of catecholamines, mainly epinephrine and norepinephrine, which stimulate adrenergic receptors, including those within the cardiovascular system. Although the most common cardiovascular manifestation is hypertension, patients with pheochromocytoma can present with arrhythmia, hypotension, shock, myocardial ischemia, cardiomyopathy, aortic dissection, and peripheral ischemia. The medical management of the cardiovascular effects of pheochromocytoma is via blockade of adrenergic receptors, usually through the use of alpha blockers, with the addition of beta blockers if needed. However, only surgical resection of the pheochromocytoma is potentially curative, and this tumor requires unique management perioperatively. Because of the variability of presentation and the significant morbidity and mortality of patients with an undiagnosed pheochromocytoma, this entity should not be overlooked in the evaluation of patients with a wide variety of cardiovascular disorders.

Phaeochromocytoma [corrected] crisis is an endocrine emergency associated with significant mortality. There is little published guidance on the management of phaeochromocytoma [corrected] crisis. This clinical practice update summarizes the relevant published literature, including a detailed review of cases published in the past 5 years, and a proposed classification system. We review the recommended management of phaeochromocytoma [corrected] crisis including the use of alpha-blockade, which is strongly associated with survival of a crisis. Mechanical circulatory supportive therapy (including intra-aortic balloon pump or extra-corporeal membrane oxygenation) is strongly recommended for patients with sustained hypotension. Surgical intervention should be deferred until medical stabilization is achieved.

Clinical expression of phaeochromocytoma may involve numerous cardiovascular manifestations, but usually presents as sustained or paroxysmal hypertension associated with other signs and symptoms of catecholamine excess. Most of the life-threatening cardiovascular manifestations of phaeochromocytoma, such as hypertensive emergencies, result from a rapid and massive release of catecholamines from the tumour. More rarely, patients with phaeochromocytoma present with low blood pressure or even shock that may then precede multisystem crisis. Sinus tachycardia, with palpitations as the presenting symptom, is the most prevalent abnormality of cardiac rhythm in phaeochromocytoma, but tumours can also be associated with more serious ventricular arrhythmias or conduction disturbances. Reversible dilated or hypertrophic cardiomyopathy are well established cardiac manifestations of phaeochromocytoma, with more recent attention to an increasing number of cases with Takotsubo cardiomyopathy. This review provides an update on the cause, clinical presentation and treatment of the cardiovascular manifestations of phaeochromocytoma. As the cardiovascular complications of phaeochromocytoma can be life-threatening, all patients who present with manifestations that even remotely suggest excessive catecholamine secretion should be screened for the disease.

Endogenous or exogenous catecholamines can induce pulmonary edema (PE). This may occur in human pathologic conditions such as in pheochromocytoma or in neurogenic pulmonary edema (NPE) but can also be provoked after experimental administration of adrenergic agonists. PE can result from stimulation with different types of adrenergic stimulation. With α-adrenergic treatment, it develops more rapidly, is more severe with abundant protein-rich fluid in the alveolar space, and is accompanied by strong generalized inflammation in the lung. Similar detrimental effects of α-adrenergic stimulation have repeatedly been described and are considered to play a pivotal role in NPE or in PE in patients with pheochromocytoma. Although β-adrenergic agonists have often been reported to prevent or attenuate PE by enhancing alveolar fluid clearance, PE may also be induced by β-adrenergic treatment as can be observed in tocolysis. In experimental models, infusion of β-adrenergic agonists induces less severe PE than α-adrenergic stimulation. The present paper addresses the current understanding of the possible contribution of α- and β-adrenergic pathways to the development of PE.

The dangers of phaeochromocytomas are mainly due to the capability of these neuroendocrine tumours to secrete large quantities of vasoactive catecholamines, thereby increasing blood pressure and causing other related adverse events or complications. Phaeochromocytomas are often missed, sometimes only becoming apparent during therapeutic interventions that provoke release or interfere with the disposition of catecholamines produced by the tumours. Because phaeochromocytomas are rare, evidence contraindicating use of specific drugs is largely anecdotal or based on case reports. The heterogeneous nature of the tumours also makes adverse reactions highly variable among patients. Some drugs, such as dopamine D(2) receptor antagonists (e.g. metoclopramide, veralipride) and beta-adrenergic receptor antagonists (beta-blockers) clearly carry high potential for adverse reactions, while others such as tricyclic antidepressants seem more inconsistent in producing complications. Other drugs capable of causing adverse reactions include monoamine oxidase inhibitors, sympathomimetics (e.g. ephedrine) and certain peptide and corticosteroid hormones (e.g. corticotropin, glucagon and glucocorticoids). Risks associated with contraindicated medications are easily minimised by adoption of appropriate safeguards (e.g. adrenoceptor blockade). Without such precautions, the state of cardiovascular vulnerability makes some drugs and manipulations employed during surgical anaesthesia particularly dangerous. Problems arise most often when drugs or therapeutic procedures are employed in patients in whom the tumour is not suspected. In such cases, it is extremely important for the clinician to recognise the possibility of an underlying catecholamine-producing tumour and to take the most appropriate steps to manage and treat adverse events and clinical complications.

Pheochromocytoma may lead to important emergency situations, ranging from cardiovascular emergencies to acute abdomen and multiorgan failure. It is vital to think about this disease in any emergency situation when conventional therapy fails to achieve control or symptoms occur that do not fit the initial diagnosis. The importance of keeping this diagnosis in minds is underscored by the fact that, in 50% of pheochromocytoma patients, the diagnosis is initially overlooked. Two other tumors of the sympathetic nervous system, neuroblastoma and ganglioneuroma, are less commonly associated with emergency conditions. If they occur, they are often linked to catecholamine excess, paraneoplastic phenomena, or local tumor mass effect.

Multiple endocrine neoplasia (MEN) type 2B is a rare hereditary disorder characterized by medullary thyroid carcinoma, pheochromocytoma, and neuroma. Early signs of MEN 2B are usually neuroma, gastrointestinal problems, and medullary thyroid carcinoma. Noncardiogenic pulmonary edema is rare as a presenting symptom. We report a 31-year-old male who was admitted to our hospital because of noncardiogenic pulmonary edema. He was 168 cm in height, weighed 55 kg, and had an arm span of 166 cm. No marfanoid habitus was evident, but thickened lips and tongue neuroma were present. Chronic constipation had been present since childhood, and the patient had a two-year history of untreated hypertension. Noncardiogenic pulmonary edema and toxic megacolon were noted, and abdominal computed tomography revealed bilateral adrenal tumors. Ultrasonography of the thyroid showed two mass lesions. Intubation and mechanical ventilation were performed because of severe hypoxemia. Endocrinological examinations showed high levels of serum and urinary fractionated catecholamines, serum calcitonin, serum carcinoembryonic antigen, and serum intact parathyroid hormone. It was suggested that the high level of catecholamine from pheochromocytoma had caused the pulmonary edema. RET gene analysis showed a codon 918 mutation in exon 16 resulting in an ATG (methionine) to ACG (threonine) substitution, but analysis of the patient's parents showed the wild type. Therefore, the patient was diagnosed as having de novo MEN 2B. He underwent laparoscopic bilateral adrenectomy and total thyroidectomy. However, the values of serum calcitonin and CEA did not decrease to the normal ranges. Patients with early-stage MEN 2B have distinct characteristics that can aid early detection of the disease, thus possibly allowing them to be saved.

Phaeochromocytoma crisis is a life-threatening emergency that may be undiagnosed because of its numerous, nonspecific manifestations. We analysed, retrospectively, the presentation, management and outcome of patients who were admitted to our institution with phaeochromocytoma crises over a 5-year period.

Five patients (two males, three females; mean age 34.6 years, range 19-51 years) who presented as emergencies requiring intensive care, with multiple non-specific manifestations and previously undiagnosed pheochromocytoma, were identified. The initial presentation included features of cardiomyopathy (n = 3), atypical pneumonia with myocarditis (n = 1) and acute abdomen (n = 1). Only one of the five cases had a raised blood pressure at the time of the acute presentation. Initiation of beta blockers in four patients was associated with further deterioration in haemodynamic status, labile blood pressure and cardiac arrhythmias, which led to the diagnosis of the underlying phaeochromocytoma. Following intensive supportive therapy and alpha blockade, all five patients recovered and underwent elective surgical removal of phaeochromocytoma, uneventfully.

Unexplained cardiopulmonary dysfunction, particularly after the institution of beta blockers, should alert clinicians to the possibility of phaeochromocytoma. A high index of suspicion is essential to reduce morbidity and mortality in these patients through early diagnosis and aggressive management.

We report a case of recurrent shock induced by pheochromocytoma in a previously healthy, normotensive patient. We review pathophysiology and clinical features of shock and cardiomyopathy in patients with pheochromocytoma. We discuss diagnostic evaluation and therapy for pheochromocytoma-induced shock.

Pulmonary edema, both cardiogenic and noncardiogenic, has been reported as a manifestation of pheochromocytoma. We report a patient with pheochromocytoma complicated by acute pulmonary edema that appeared clinically noncardiogenic. The patient had an uncomplicated course and rapid resolution of pulmonary edema. Bronchoalveolar lavage fluids (BALF) showed a marked accumulation of neutrophils, suggesting involvement of neutrophil-mediated lung injury in noncardiogenic pulmonary edema associated with a pheochromocytoma.

Stimulation with norepinephrine (NE) leads to pulmonary edema and pleural effusion in rats. These pulmonary fluid shifts may result from pulmonary congestion due to the hemodynamic effects of NE and/or inflammation with an increase in vascular permeability. The contribution of these two factors were investigated in the present study. Female Sprague-Dawley rats received continuous i.v. NE infusion (0.1 mg/kg/h) over time intervals between 90 min and 72 h. After heart catheterization, pleural fluid (PF) and lung tissue were obtained. In some of the animals, a bronchoalveolar lavage (BAL) was performed. Pulmonary edema and inflammation were shown histologically. We determined the expression of interleukin (IL)-6 as one of the most potent acute-phase protein mediators in serum, PF and BAL supernatant fluid (BALF) using ELISA as well as in the lung tissue using Western blotting. Total protein concentration in BALF and PF served as indicators of increased capillary permeability. Pulmonary edema and pleural effusion appeared coincidentally with an increase in total peripheral resistance (TPR) after 6 h of NE infusion. PF reached a maximum between 8 and 16 h (2.2 +/- 0.3 ml, controls < 0.5 ml) and disappeared within 48 h. Activation of IL-6 in the fluids was observed after 8 h of NE stimulation. In the lung tissue it started after 12 h and reached 330% of the control value after 48 h. Pulmonary inflammation was documented histologically. It was accompanied by increased protein concentration in BALF after 24 h of NE treatment. Hemodynamic effects of NE are the main causative factors in the initial phase of the pulmonary fluid shifts. Additionally, NE leads to an activation of cytokines such as IL-6 and to inflammation and to an increase in capillary permeability. However, inflammation and increased capillary permeability occurred later than pulmonary edema and pleural effusion. Hence, we conclude that they are secondary factors which may contribute to maintain the fluid shifts over a longer period of time.

We investigated the contribution of alpha- and beta-adrenergic pathways to catecholamine-induced pulmonary edema and the role of pleural effusion in preventing alveolar edema. Female Sprague-Dawley rats received continuous intravenous infusion of norepinephrine and of separate alpha- or beta-adrenergic stimulation over 6-24 h. We performed heart catheterization in vivo and excised post mortem lung tissue for histological analysis. Interleukin (IL)-6 and total protein concentrations were determined in serum, pleural fluid (PF) and bronchoalveolar lavage fluid. alpha-Adrenergic treatment increased right ventricular systolic pressure (RVSP) and total peripheral resistance (TPR) and caused severe alveolar edema associated with IL-6 activation in serum and diffuse pulmonary inflammation. PF amounts were moderate (0.9+/-0.2 ml). beta-Adrenergic stimulation also increased RVSP but decreased TPR. Interstitial but not alveolar edema and focal inflammation without IL-6 activation developed. Large PF amounts (6.2+/-1.5 ml) occurred which were considered to prevent alveolar edema. We conclude that both alpha- and beta-adrenergic stimulation contribute to pulmonary fluid shifts in rats, but alpha-adrenergic pathways cause more acute and more severe lung injury than beta-adrenergic mechanisms.

Pheochromocytomas cause the most dramatic, life-threatening crises in all of endocrinology. Pheochromocytoma is an explosive clinical syndrome characterized by severe hypertension associated with cardiac complications, hypotension, or even shock and sudden death. The key to diagnosing pheochromocytoma is to suspect it, then confirm it. The cases reported in this review illustrate how the diagnosis can be easily missed and definitive treatment delayed. An appreciation of the wide range of clinical manifestations, based on clear understanding of the mechanisms of catecholamine action and the pathophysiology of pheochromocytoma, and the availability of simple and accurate diagnostic tests should lead to earlier detection of these tumors. Advances in localization techniques and availability of various treatment modalities have made successful management more promising than ever before.

This report describes the perioperative management of an adrenergic crisis occurring following insufflation of the peritoneum for planned laparoscopic surgery for phaechromocytoma. Despite preoperative alpha and beta adrenergic blockade, the occurrence of acute severe hypertension, mydriasis and pulmonary oedema prior to direct surgical manipulation caused the procedure to be abandoned. The severity of the event was unusual and most likely contributed to by haemorrhagic necrosis of the tumour releasing catecholamines. Serum levels of noradrenaline and adrenaline at the time were 744,600 and 166,940 pg.ml-1 respectively. Treatment included bolus doses of esmolol, nicardipine and urapidil (an alpha 1 adrenergic antagonist) by constant intravenous infusion and mechanical ventilation. Postoperative cerebral CT scan was normal. An abdominal CT showed central haemorrhagic necrosis of the tumour. Two weeks later, open surgical removal of the phaeochromocytoma was successfully performed under general anaesthesia. Induction of pneumoperitoneum for laparoscopy may be particularly hazardous in a patient with a phaeochromocytoma.

Pulmonary manifestations of pheochromocytoma are infrequent and are not well documented. A MEDLINE search in the English language revealed no cases of endobronchial involvement from a pheochromocytoma. We report a case of endobronchial metastases in a 37-year-old woman known to have a recurrent extra-adrenal pheochromocytoma. She presented with symptoms of wheezing and a nonproductive cough for 8 months and was being treated for asthma. A flexible bronchoscopy with endobronchial biopsy established the diagnosis. The patient underwent a Nd-YAG laser photoresection (LPR) to ablate the tumor, which was followed by placement of a Wallstent (Pfizer Medical Technology Group; Rutherford, NJ). She remains well 18 months later, having required multiple palliative LPRs. To our knowledge, this is the first reported case of endobronchial pheochromocytoma. The pulmonary manifestations of this rare disease and their management are reviewed.

Pheochromocytoma is a rare tumor that secretes excess catecholamines. Pheochromocytoma crises may be precipitated by the use of several drugs. This article describes the case of a patient affected by pheochromocytoma in whom multiple organ failure developed after contemporary administration of ergotamine, caffeine, and nimesulide. The patient recovered completely long after surgical intervention.

Phaeochromocytomas are rare tumours that most commonly present with chronic sustained hypertension and hypertensive paroxysms or crises. We report a 49-year-old woman with unsuspected phaeochromocytoma who presented with sudden onset of profound hypotension and adult respiratory distress syndrome unresponsive to fluid and inotropic support. This case illustrates the diversity of presentations of phaeochromocytoma, depending on the type and amount of catecholamines secreted.

Most patients with hypertension in the United States have essential (primary) hypertension (95%), the cause of which is unknown. The remaining 5% of adults with hypertension have the secondary form of hypertension, the cause and pathophysiologic process of which are known. Internists and other primary care physicians refer to this as treatable or curable hypertension, because the hypertension can be managed or even controlled with medications. Similarly, the condition is called surgical hypertension by surgeons in the belief that once the cause is determined and identified, surgical intervention will result in cure of hypertension. Secondary causes of hypertension include renal parenchymal disease, renovascular diseases, coarctation of the aorta, Cushing's syndrome, primary hyperaldosteronism, pheochromocytoma, hyperthyroidism, and hyperparathyroidism. Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. The evaluation of secondary hypertension is of interest and can bring together different facets of anatomy, physiology, pharmacology, and radiology in the medical and surgical treatment of these disorders. Despite enthusiasm that can be generated in the evaluation of these conditions, evaluation can be expensive and should not be conducted for all patients with hypertension. Features that aid in the diagnosis of secondary hypertension include the following: 1. Onset of hypertension before the age of 20 or after the age of 50 years. The presence of hypertension at a young age may suggest coarctation of the aorta, fibromuscular dysplasia, or an endocrine disorder. Hypertension found for the first time after the age of 50 years may suggest the presence of renovascular hypertension caused by atherosclerosis. 2. Markedly elevated blood pressure or hypertension with severe end-organ damage, as in grade III or IV retinopathy. These findings suggest the presence of renovascular hypertension or pheochromocytoma. 3. Specific body habitus and ancillary physical findings. For example, truncal obesity and purple striae occur with hypercortisolism, and exophthalmos is associated with hyperthyroidism. 4. Resistant or refractory hypertension (poor response to medical therapy usually necessitating use of more than three antihypertensive medications from three different classes). 5. Specific biochemical test that suggest the existence of certain disorders, such as hypercalcemia in hyperparathyroidism, hyperglycemia in Cushing's syndrome and pheochromocytoma, and unprovoked hypokalemia with renin-producing tumors, primary hyperaldosteronism, or renin-mediated renovascular hypertension. 6. Other characteristics that may suggest secondary hypertension such as abdominal diastolic bruits (renovascular hypertension), decreased femoral pulses (coarctation of the aorta), or bitemporal hemianopias (Cushing's disease). A combination of a good history and physical examination, astute observation, and accurate interpretation of available data usually are helpful in the diagnosis of a specific causation.

A patient presented with apparent septicaemic shock. Full invasive cardiovascular monitoring revealed systemic hypotension, high normal cardiac output, and a low systemic vascular resistance. Maintenance of systemic vascular resistance and blood pressure was shown to be highly dependent on noradrenaline. Subsequent investigation revealed the presence of a phaeochromocytoma producing adrenaline. The mechanisms by which phaeochromocytomas may produce hypotension are discussed.

Phaeochromocytoma may present as an acute emergency with a perplexing variety of symptoms. We report a case in which a tumour of the organ of Zuckerkandl was removed after its unexpected discovery during laparotomy for abdominal trauma. A patient is described in whom a history of abdominal trauma coupled with collapse, pulmonary oedema, raised serum amylase and a positive peritoneal tap for blood, led to laparotomy at which an extramedullary phaeochromocytoma was found unexpectedly. The tumour was successfully resected, but immediate hypotension was life threatening. The inadvisability of resecting a phaeochromocytoma discovered at operation is discussed.