If the renal arteries are stenosed, blood has difficulty reaching the kidneys. That is, both are poorly perfused and can only create the pressure gradient necessary for filtration by contraction of the efferent arteriole. If we administer an ACEI, we will provoke the relaxation of this arteriole and the fall of the glomerular filtration rate. And if neither kidney filters, because both have arterial stenosis, we have a problem....

A 45-year-old woman presents arterial hypertension (190/120 mmHg) accompanied by K 2.5 mEq/l. An abdominal ultrasound shows stenosis of both renal arteries. Indicate which treatment is contraindicated:

[Hypertensive crisis in a 3-year-old boy - neurovascular conflict?]

Hypertensive crisis is a sudden rise in blood pressure with accompanying clinical symptoms. The disease is extremely rare in small children and is always a complication of secondary hypertension. 3-year-old boy (spontaneous delivery, 37 week of gestation, birth weight 2170g, 10 AS, unremarkable family history) was admitted to a hospital because of weight loss (1.5 kg, i.e. approx. 15% in 6 months), anorexia, abdominal and limb pain and lethargy. On admission, very high blood pressure values (190/150 mm Hg), lean subcutaneous tissue, frequent blinking, height 88 cm (<3c), body weight 9.5 kg (<3c). In additional tests: blood morphology, parameters of renal function, ions, gasometry, catecholamine urinary excretion, steroid profile and daily cortisol profile were within normal limits. Elevated plasma renin activity was found. In imaging studies kidneys, adrenal glands and renal arteries were normal. Normotension was not obtained on two antihypertensive drugs - metoprolol and amlodipine. In angio-CT tortuous right vertebral artery, extending to the left on the anterolateral surface of the medulla oblongata - possible compression of the vessel of the left side of medulla - was found. Diagnosis of neurovascular conflict was made. The patient was consulted by neurosurgeon who declare no possibility of surgical treatment of anomalies. In the treatment, according to the literature, a drug blocking the renin-angiotensin-aldosterone-enalapril system was used, which normalized blood pressure. At the same time, intensive nutritional treatment was used. Resolution of symptoms and weight gain was observed. In further follow-up patients' parents withdrew enalapril lawlessly, which did not lead to recurrent rise in blood pressure. The latter may suggest other, transient cause of hypertensive crisis e.g. intoxication. Severe hypertension in pediatric patients can give symptoms as weight loss and behavioral disorders. In the diagnostic of hypertensive crisis in children, neuroimaging studies and toxicological tests should be performed.

Resistance to antihypertensive medication as predictor of renal artery stenosis: comparison of two drug regimens.

Renal artery stenosis is among the most common curable causes of hypertension. The definitive diagnosis is made by renal angiography, an invasive and costly procedure. The prevalence of renal artery stenosis is less than 1% in non-selected hypertensive patients but is higher when hypertension is resistant to drugs. To study the usefulness of standardised two-drug regimens for identifying drug-resistant hypertension as a predictor of renal artery stenosis. Prospective cohort study carried out in 26 hospitals in The Netherlands. Patients had been referred for analysis of possible secondary hypertension or because hypertension was difficult to treat. Patients < or =40 years of age were assigned to either amlodipine 10 mg or enalapril 20 mg, and patients >40 years to either amlodipine 10 mg combined with atenolol 50 mg or to enalapril 20 mg combined with hydrochlorothiazide 25 mg. Renal angiography was performed: (1) if hypertension was drug-resistant, ie if diastolic pressure remained > or =95 mm Hg at three visits 1-3 weeks apart or an extra drug was required, and/or (2) if serum creatinine rose by > or =20 micromol/L (> or =0.23 mg/dL) during ACE inhibitor treatment. Of the 1106 patients with complete follow-up, 1022 had been assigned to either the amlodipine- or enalapril-based regimens, 772 by randomisation. Drug-resistant hypertension, as defined above, was identified in 41% of the patients, and 20% of these had renal artery stenosis. Renal function impairment was observed in 8% of the patients on ACE inhibitor, and this was associated with a 46% prevalence of renal artery stenosis. In the randomised patients, the prevalence of renal artery stenosis did not differ between the amlodipine- and enalapril-based regimens. In the diagnostic work-up for renovascular hypertension the use of standardised medication regimens of maximally two drugs, to identify patients with drug-resistant hypertension, is a rational first step to increase the a priori chance of renal artery stenosis. Amlodipine- or enalapril-based regimens are equally effective for this purpose.

Arterial hypertension with brachydactyly in a 15-year-old boy.

Autosomal dominant brachydactyly with hypertension is the only form of monogenic hypertension which is not sodium dependent. The disease is characterized by brachydactyly type E, short stature, arterial hypertension and aberrant loop of posterior inferior cerebellar artery (PICA) causing neurovascular conflict. So far the syndrome was described in one family in Turkey and two in Canada. We report a case of a 15-year-old boy who was admitted because of arterial hypertension 160/100 mmHg. He complained also of attacks of bilateral numbness of hands with deterioration of visual field. Examination revealed short stature (156 cm) and bone deformities of hands and feet consistent with brachydactyly type E. Ophthalmoscopy showed mild narrowing of retinal arteries. Serum electrolytes, blood gases, and renal function were normal. Renin activity and aldosterone concentrations were raised, and 24-h urinary excretion of catecholamines and urinary steroid profile were in normal range. Renal Doppler ultrasound was normal, but renal scintigraphy suggested vascular changes in the left kidney. Echocardiographic examination, besides mild left ventricular hypertrophy, was normal. Magnetic resonance angiography (angio-MR) revealed bilateral abnormal PICA loops and neurovascular conflict. Spiral angiotomography of renal arteries revealed narrow additional left renal artery. Both nonconsanguineous parents and younger brother were healthy, with normal height, without bone deformities, and had normal intracranial vessels. Amlodipine and metoprolol were given, and blood pressure lowered to 143/87. Adding rilmenidine gave no effect and enalapril was then added. It led to further improvement in blood pressure control. To our knowledge, this is the first pediatric description of a sporadic form of autosomal dominant brachydactyly with hypertension with abnormalities of brain and renal arteries.

[Comparative evaluation of the antihypertensive efficacy of amlodipine versus enalapril].

Goal of this study was to compare the efficacy and safety of amlodipine with enalaprile in case of patients with moderate essential arterial hypertension. Study involved 40 patients with hypertension, 22 males and 18 females, age 39-80 years. Diastolic blood pressure was from 100-120 mmHg. Patients were for two weeks without any therapy and after that were divided into two groups of 20, fortherapy with amlodipine or enalaprile. The patients received 5-10 mg of amlodipine or enalaprile once daily. Initial blood pressure, before therapy was similar in groups, 173.00/108.00 mmHg and 175.25/106.75 mmHg (mean value). After four weeks on treatment the BP was reduced in both groups, in group on amlodipine from 173.00/108.00 to 129.75/78.50 mmHg (mean value), and in the group on enalaprile from 175.25/106.75 to 133.50/81.50 mmHg. Patients did not report any side effects in either of the groups. We prove that one day therapy with small doses, 5-10 mg of amlodipine, new calcium channels blocker and enalaprile, ACE inhibitor were efficient and safe in therapy of the essential hypertension. We found that amlodipine was somewhat more efficient than enalaprile in lowering the blood pressure.

[Case of fibromuscular dysplasia revealed by the emergence of severe hypertension in the early phase of pregnancy].

A 25-year-old female at 10 weeks of her first pregnancy abruptly developed severe hypertension as high as 230/160 mmHg and thus was referred to our hospital. Her past history was unremarkable and no medication or supplement was prescribed. The laboratory findings revealed that plasma renin activity was 59.0 ng mL hr and plasma aldosterone concentration was 1700 pg mL together with serum creatinine of 0.42 mg dL and serum potassium of 2.8 mEq L. Urinalysis revealed insignificant findings. Her hypertension was extremely resistant to antihypertensive agents, including hydralazine, alpha-methyldopa, and alpha beta blocker, leading to suspicion of secondary hypertension as a cause. Adrenal tumor was not detected but Doppler ultrasonography suggested the constriction of the right renal artery consistent with renovascular hypertension. Considering the following imaging test and medications, the patient and her family decided to abort the pregnancy. 3D-CT and MR angiography showed stenosis of the right renal artery, therefore, percutaneous transcatheter renal angioplasty was performed, resulting in normalization of the blood pressure without antihypertensives. Two years later she successfully gave birth uneventfully. Her hypertension was presumably irrelevant to preeclampsia because it occurred at 10 weeks of pregnancy and proteinuria was not associated. The stenosis of the right renal artery was probably due to fibromuscular dysplasia, which is one of the major causes of renal artery stenosis in young women. This patient was such a case and presented a difficult decision on how to treat and whether or not to abort. We will discuss the mechanism of hypertension in pregnancy and the advantages and disadvantages of available treatments for such cases.

Hyponatremic hypertensive syndrome (HHS) in an 18-month old-child presenting as malignant hypertension: a case report.

The combination of hyponatremia and renovascular hypertension is called hyponatremic hypertensive syndrome (HHS). Malignant hypertension as a presentation has been reported in adults with HHS but is rare in children. An eighteen month-old male presented with drowsiness, sudden onset status epilepticus and blood pressure of 210/160. The electrolytes on admission revealed sodium of 120 mEq/L and potassium of 2.1 mEq/L. The peripheral renin activity (PRA) was 172 ng/ml/min (normal 3-11 ng/ml/min) and serum aldosterone level was 91 ng/dl (normal 4 to 16 ng/dl). Patient underwent angioplasty with no success, followed by surgical correction. Two years since the diagnosis, the blood pressure is controlled with labetolol and amlodipine (at less than sixth of the pre-operative dosages). The PRA is 2.4 ng/ml/min and aldosterone 15.5 ng/dl. The child not only had three renal arteries on left but all of them were stenosed which to best of our knowledge has not been described. As uncommon as HHS with malignant hypertension may be in adults it is under-reported in children and purpose of the case report is to raise its awareness.

Unique imaging findings in fibromuscular dysplasia of renal arteries: A case report.

Fibromuscular dysplasia (FMD) is a rare vascular disorder that causes abnormal cell growth in arterial walls. The classic "string of beads" sign has been reported in many cases, whereas the appearance of tubular stenosis and distal tapering of renal arteries with multiple renal infarctions, as well as left kidney atrophy occurring in one patient, has not been precisely described. A 19-year-old woman presented to us with a history of elevated blood pressure without any symptoms for the past 1 month. Routine laboratory tests indicated a moderately impaired renal function, and ultrasound examination demonstrated a small-sized left kidney and seriously decreased blood flow of the left renal artery and its branches. Subsequent contrast-enhanced computed tomographic angiography (CTA) demonstrated multiple ischemic infarctions in the bilateral kidneys, and FMD was suggested at that time. Thereafter, we performed selective reno-angiography, which confirmed that the all left renal arteries had tubular stenosis and that right renal arterial branches presented distal tapering. Antihypertensive drugs were prescribed conservatively, including nifedipine 60 mg/d and prazosin 4 mg/d, to lower the patient's blood pressure. The patient had a well-controlled blood pressure and an improved renal function at her 6-month follow-up. We should take the diagnosis of FMD into account if young women develop asymptomatic hypertension. To our knowledge, this is the first case that exhibited renal artery FMD manifesting as tubular stenosis and distal tapering, especially followed by bilateral renal infarctions and significant atrophy of the left kidney. In addition, CTA combined with digital subtraction angiography (DSA) may be more sensitive than other tests with respect to the detection of intrarenal infarctions and arterial variants of FMD.

The simultaneous occurrence of renal artery stenosis and an aldosteronoma in a patient with hypertension.

The simultaneous occurrence of renovascular hypertension and an adrenocortical adenoma is a rare entity. The case of a 64-year-old woman who underwent an aortorenal bypass graft for renovascular hypertension requiring a multidrug antihypertensive regimen is presented. Persistently elevated blood pressures in the postoperative period prompted further workup for other causes of hypertension. Laboratory evaluation showed hyperaldosteronism and hyporeninemia despite enalapril administration. Abdominal computerized tomography (CT) revealed a left adrenal mass which, on surgical removal, was found to be a cortical adenoma. Subsequently, her antihypertensive therapy has been reduced to a single agent. Previous authors have described only four patients with malignant hypertension who had the rare clinical combination of renal artery stenosis and an aldosteronoma. This case reemphasizes the critical need for a thorough search for other surgically correctable lesions in those patients who remain severely hypertensive after the "definitive" operation.

[Renovascular hypertension with renal failure: value of renal revascularization].

The purpose of this work was to determine the effects of renal revascularization on blood pressure and renal function in 9 patients with arterial stenosis involving both kidneys (7) or a solitary kidney (2). There were five women and four men with a mean (SD) age for 64.5 +/- 7 years. The duration of hypertension ranged from 2 to 28 years (mean = 12 +/- 8). Blood pressure ranged from 210/100 to 260/150 mmHg, despite the use of three or more antihypertensive agents in 7 cases. The serum creatinine level, on presentation, ranged from 160 to 265 mumol/l (mean = 198 +/- 30 mumol/l). Intravenous pyelograms were not suggestive of renovascular disease in 4 of 7 cases. Digital angiography or arteriography demonstrated severe stenosis of the artery of the solitary kidney in 2 patients, severe bilateral atherosclerotic disease in 7 patients, three of them had complete occlusion of a main renal artery. During hospitalization, therapy with captopril (5 patients) or minoxidil (1 patient) lowered blood pressure in 3 cases, but induced a marked increase in serum creatinine level in 4 cases. In two patients, medically treated, severe and rapidly progressive impairment of renal function was observed. The seven remaining patients underwent surgical revascularization (two after unfructuous percutaneous transluminal angioplasty). One died 45 days later. Blood pressure control with diastolic blood pressure of 100 mmHg or less was achieved in the other six, although each patient continued to require antihypertensive medication (bitherapy: 2, monotherapy: 4).(ABSTRACT TRUNCATED AT 250 WORDS)

[Hypoplasia of the renal artery as a cause of renovascular hypertension. A case report].

The authors report the case of an 8-year-old Libyan boy who presented with hypertension, episodes of vomiting and headaches during the past year. Routine blood tests, including nitrogen and urea clearances, were normal; an ultrasound scan and a urography demonstrated a left kidney smaller than the right. Further tests were carried out to evaluate the morphology and the function of the kidney; a scintigraphy confirmed the hypoplasia of the left kidney with reduction of the glomerular filtration rate. The arteriography of the abdominal aorta was decisive, confirming not only the hypoplasia of the left kidney, but also the presence of a hypoplasic renal artery. The latter appeared to be uniformly hypoplasic, with no signs of segmentary stenosis. This fact suggested the hypothesis of renovascular hypertension caused by a hypoplasia of the renal artery. The medical treatment with enalapril gave good results, with normalization of the pressure levels after 5 days of administration. However, only nephrectomy is able to give excellent long-term results.

Management of severe hypertension in a child with tuberous sclerosis-related major vascular abnormalities.

We report the case of a 4-year-old girl with tuberous sclerosis who presented with severe renovascular hypertension secondary to compression of the renal arteries by a large infradiaphragmatic abdominal aortic aneurysm. Case report of a previously unreported case. Normotension could not be achieved despite conservative treatment with three antihypertensive drugs at high doses. An aortic graft was performed successfully but failed to correct the hypertension. Postoperatively, the child experienced acute renal failure after attempting treatment with additional enalapril. Further investigations revealed ischaemia of the left kidney and stenosis of the right renal artery. Subsequently, a combination of maximum dose minoxidil, a calcium antagonist, clonidine and peripheral alpha and beta-blockers, and diuretics was used, but her blood pressure control remained poor. A bypass between the hepatic artery and the right renal artery restenosed at the proximal anastomosis. Her renovascular hypertension was finally improved with an autotransplantation of her right kidney into the right iliac fossa. Fibromuscular dysplasia and abundant collagen deposition were the predominant features seen on histology. She is currently normotensive on moderate doses of a beta-blocker, amlodipine and a diuretic. Hypertension in this case was impossible to control medically, and the surgical approach was compromised by numerous complications. This case illustrates the challenges in the management of renovascular hypertension in a child with disease-associated vascular malformations.

Hypertensive urgency

In a hypertensive urgency blood pressure should be lowered carefully to ≤160/≤100 mmHg over a period of hours to days, this can often be done as an outpatient. There is limited evidence regarding the most appropriate rate of blood pressure reduction, although it is recommended that mean arterial pressure should be lowered by no more than 25 to 30 percent over the first few hours. Recommended medications for hypertensive urgencies include: captopril, labetalol, amlodipine, felodipine, isradipine, and prazosin. Sublingual nifedipine is not recommended in hypertensive urgencies. This is because nifedipine can cause rapid decrease of blood pressure which can precipitate cerebral or cardiac ischemic events. There is also lack of evidence on the benefits of nifedipine in controlling hypertension. Acute administration of drugs should be followed by several hours of observation to ensure that blood pressure does not fall too much. Aggressive dosing with intravenous drugs or oral agents which

Case Study: 8-Year-Old With a Murmur and Hypertension -- Management

In the ED, nifedipine was given once for hypertension, and her blood pressure responded appropriately. The patient also had a 4/5 headache that was treated with acetaminophen and ibuprofen, and it improved. Nephrology was consulted. The specialist recommended a renal ultrasound and other labs as well as starting amlodipine 5 mg daily. The patient was admitted to the hospital for further management. [4] [5] [6]

Hypertensive encephalopathy

Once the BP is controlled, the person should be switched to medication by mouth, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months. The initial reduction to a diastolic pressure of approximately 100 mmHg is often associated with a modest worsening of renal function; this change, however, is typically transient as the vascular disease tends to resolve and renal perfusion improves over one to three months. Antihypertensive therapy should not be withheld in this setting unless there has been an excessive reduction in BP. A change in medication, however, is indicated if the decline in renal function is temporally related to therapy with an angiotensin (ACE) converting enzyme inhibitor or angiotensin II receptor blocker, which can interfere with renal autoregulation and produce acute kidney failure in patients with bilateral renal artery stenosis. (See "Renal effects of ACE inhibitors in hypertension".)ref

[Hypotensive properties of nisoldipine. Comparative study in essential, renal and renovascular hypertension].

Calcium antagonists are increasingly used in the treatment of primary and secondary hypertension. A new substance of this group, isobutyl methyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinecarboxylate (nisoldipine, Bay k 5552) inhibits the calcium-induced contraction of arteries and veins in concentrations 5-20 times lower compared to those of nifedipine in vitro. The effect of nisoldipine (10 mg orally) on blood pressure and heart rate in supine and upright position, on serum electrolytes (Na+, K+, Ca2+) and on serum aldosterone and serum hydrocortisone (cortisol) was comparatively studied in patients with essential hypertension (n = 6, 57 +/- 7 years), in patients with hypertension and chronic renal failure (n = 6, 46 +/- 4 years, serum creatinine 2.1 +/- 0.5 mg/100 ml) and in 6 patients with unilateral renal artery stenosis. In patients with essential hypertension, systolic blood pressure (BP) dropped by 26 mmHg; diastolic BP was lowered by 17 mmHg after 150 min compared to placebo. In patients with chronic renal failure, decrement in BP was 25/16 mmHg (systolic and diastolic BP, respectively). In patients with renal artery stenosis, blood pressure declined by 31/18 mmHg after nisoldipine. Serum electrolytes (Na+, K+ and Ca2+) and serum aldosterone as well as serum hydrocortisone remained unchanged. The hypotensive action of nisoldipine seems to be independent of the type of hypertension. However, the hypotensive activity correlates with the level of the baseline blood pressure.

Renal artery

Clinical significance Stenosis Renal artery stenosis, or narrowing of one or both renal arteries will lead to hypertension as the affected kidneys release renin to increase blood pressure to preserve perfusion to the kidneys. RAS is typically diagnosed with duplex ultrasonography of the renal arteries. It is treated with the use of balloon angioplasty and stents, if necessary. Atherosclerosis Atherosclerosis can also affect the renal arteries and can lead to poor perfusion of the kidneys leading to reduced kidney function and, possibly, renal failure. Trauma A renal artery is damaged in 4% of blunt traumas and 7% of penetrating traumas to the abdomen. Additional images References External links - "Posterior Abdominal Wall: Branches of the Abdominal Aorta" Arteries of the abdomen

Hypokalemia induced myopathy as first manifestation of primary hyperaldosteronism - an elderly patient with unilateral adrenal hyperplasia: a case report.

Primary hyperaldosteronism is only rarely caused by unilateral adrenal hyperplasia. A 73-year-old hypertensive Greek man (on 10 mg amlodipine for the last ten years) presented in the emergency department with severe muscle weakness of all limbs. The initial physical and laboratory examination revealed normal blood pressure, muscle weakness, severe hypokalemia, sinus rhythm and U wave, rhabdomyolysis and metabolic alkalosis. The patient was immediately treated with intravenous administration of potassium-rich solutions, 25 mg spironolactone with progressive dose titration up to 100 mg. Because of high arterial blood pressure, irbesartan was added. On day 6, muscle weakness was completely restored with decrease of arterial blood pressure and further improvement of laboratory tests. The combination of hypokalemia with arterial hypertension raised the suspicion of primary hyperaldosteronism; therefore, we performed abdomen computed tomography scan, which revealed a nodular mass (15 mm in diameter) in the left adrenal gland. Plasma renin activity was in the lower normal range with a three-fold increase of plasma aldosterone concentration. We performed total resection of the left adrenal gland and the histopathological examination revealed hyperplasia of the left adrenal gland. This report presents a rare case of an elderly patient under antihypertensive treatment the last ten years for essential hypertension, who admitted to our emergency department with hypokalemia - induced myopathy as first manifestation of primary hyperaldosteronism due to unilateral adrenal hyperplasia.

Renal artery stenosis

Changes include: Fibrosis Tubular cell size (decrease) Thickening of Bowman capsule Tubulosclerosis Glomerular capillary tuft (atrophy) Diagnosis The diagnosis of renal artery stenosis can use many techniques to determine if the condition is present, a clinical prediction rule is available to guide diagnosis. Among the diagnostic techniques are: Doppler ultrasound study of the kidneys Refractory hypertension Auscultation (with stethoscope) - bruit ("rushing" sound) Captopril challenge test Captopril test dose effect on the differential renal function as measured by MAG3 scan. Renal artery arteriogram. The specific criteria for renal artery stenosis on Doppler are an acceleration time of greater than 70 milliseconds, an acceleration index of less than 300 cm/sec² and a velocity ratio of the renal artery to aorta of greater than 3.5. Treatment

[Refractory hypertention in a female patient with renal failure].

We report one sixty-seven years-old female who presented with hypertension refractory to antihypertensive drugs. She had an elevated BP for approximately 15 years. In the last 8-10 months her hypertension had become difficult to control. Her BP ranged between 180/100 mmHg and 220/1220 mmHg on atenolol 100 mg once daily, methyldopa 500 mg three times daily, furosemide 25 mg twice daily, doxazosine 4 mg twice daily. When she was referred to our unit serum creatinine was 2.3 mg/dL and she had a mild proteinuria (70 mg/dL) without microematuria. Ultrasonography showed a left kidney size in the low-normal range (LD 11 cm) and a small right kidney (LD 9 cm). Renal angiography showed a severe, ostial stenosis of the left renal artery and a total thrombosis of the right renal artery with a blood supply to the right kidney provided by collateral channels. An ACE-I was added to the therapy but a sharp increase in serum creatinina (up to 6.4 mg/dL) prompted us to withdraw the drug. She underwent a renal angioplasty on the left side and a Palmaz stent was placed. The control angiography showed a good anatomical result. Three months after the manoeuvre the patient was again referred to our unit with headache, nausea vomiting and hyper-tension refractory to amlodipine 10 mg/day, doxazosine 4 mg twice a a day, atenolol 50 mg/day, furosemide 50 mg/day. A doppler ultrasonography and a magnetic resonance angiogram showed no restenosis on the treated artery. An ACE-I was again administered and BP on this drug was 145/90 mmHg after one month and 130/85 after three months. Headache, nausea and vomiting disappeared. Serum creatinina kept unchanged (2.2 mg/dL). Comment. In this case the benefit of angioplasty on blood pressure control was indirect. Apparently the manoeuvre showed no effect on blood pressure, but the angioplasty allowed us to use of an ACE-Inhibitor, without any negative effect on renal function, and thus to adequately control blood pressure.

Renal artery stenosis

Renal artery stenosis (RAS) is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. This narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension – a secondary type of high blood pressure. Possible complications of renal artery stenosis are chronic kidney disease and coronary artery disease. Signs and symptoms Most cases of renal artery stenosis are asymptomatic, and the main problem is high blood pressure that cannot be controlled with medication. Decreased kidney function may develop if both kidneys do not receive adequate blood flow, furthermore some people with renal artery stenosis present with episodes of flash pulmonary edema.

Amlodipine-Induced Gingival Hyperplasia in a Young Male with Stage 5 Chronic Kidney Disease.

Gingival hyperplasia is a rare finding in clinical practice. Nevertheless, when it occurs, it is a finding of great value as it can lead to definite clinical diagnosis. The present case is a 19-year-old male who was referred for further management of stage 5 chronic kidney disease. On evaluation, he was found to have gingival hyperplasia. He was evaluated for reversible causes of kidney disease, and since none were found, renal replacement therapy was advised. He had been taking amlodipine for blood pressure control. As this was presumed to be the cause of gingival hyperplasia, it was stopped and replaced by a combination of beta-blocker and prazosin. At six-month follow-up, he had complete resolution of gingival hyperplasia. Amlodipine as a cause of gingival hyperplasia is a rare occurrence. However, it is crucial to keep in mind such a possible side effect of this commonly prescribed antihypertensive drug.

[The role of calcium inhibitors in the treatment of arterial hypertension].

Base on their own experience with isradipine and results of a multicentric study with amplodipine in the Slovak Republic, as well as based on data in the literature the authors conclude that: 1. In the treatment of arterial hypertension associated in the syndrome of insulin resistance (syndrome X and 5H resp.) with type 2 diabetes, hyperlipiproteinaemia and hyperinsulinism drugs of first choice include ACE-inhibitors and Ca antagonist of the second generation, dihydropiridine type, such as amplodipine, isradipine, fellodipine, nirtendipine etc. ACE inhibitors and Ca antagonist of the dihydropyridine type with prolonged effect have a good tolerance, few undesirable effect, a favourable effect on the decline of BP, regression of hypertrophy of the left ventricle and vascular wall; they do not cause deterioration of insulin resistance and thus do not interfere with compensation of diabetes and associated hyperlipoproteinaemia. 2. ACE inhibitors moreover reduce glomerular filtration and albuminuria and thus retard along with the effect on BP the progression of diabetic nephropathy. 3. In pre-existing hyporeninemic hypoaldosteronism (cca in 18% diabetic subjects) they can however cause dangerous hyperkalinaemia by further inhibition of the damaged renin-angiotensin-aldosterone system. In instances Ca inhibitors are indicated. The latter activate RAAS and do not have an impact on albuminuria. By their effect on the vas deferens they can increase glomerular filtration. 4. Diuretics are not suitable for the treatment of hypertension in X syndrome and the use of beta-blocking agents even with ISA and beta-1-selective preparations in restricted in particular when insulin is administered or other numerous contraindications are present (cardiac failure, bradyarrythmias, bronchitis etc.). Perhaps a combination of ACE-inhibitors and Ca antagonists of the 2nd generation with an alpha-blocking agent or hybrid alpha-beta-blocking agent is a suitable solution.

[Modern treatment of hypertension in older patients (author's transl)].

In aged people a differentiation has to be made between "arteriosklerotic hypertension" due to increased stiffness of the aorta and true hypertension in older patients. The therapy of hypertension in older patients principally is the same as in younger individuals; however, blood pressure should be lowered slowly with the respect to concomitant diseases of the kidney, coronary arteriosclerosis and heart failure. Usually, in older patients there long-standing hypertension with increased peripheral resistance and low cardiac output. Therefore, a diuretic or vasodilating agent may be the drug of first choice. Betablockers are not generally contraindicated, but given with caution. The same is true for ganglionblocking agents. In a large number of cases salt restriction and general measures will lead to a suitable blood pressure control.

Renovascular hypertension due to bilateral renal artery stenosis treated with stent implantation in a 12-year old girl.

Renovascular hypertension (RVH) in children is a relatively rare disease, but it is important in that it is a treatable condition when properly diagnosed. Percutaneous transluminal renal angioplasty (PTRA) with or without stenting is widely applied to adult patients with RVH. However, limited information is available as to PTRA with stenting in pediatric patients. We experienced a case of RVH in a 12-year-old girl, who had severe hypertension (180/110 mmHg). Bilateral renal artery stenosis was demonstrated by 3D-CT, MR angiography and selective renal arteriography. Renal function and plasma renin activity were normal. Angiotensin blockade was refrained for fear of functional deterioration of the kidney. Medical treatment with amlodipine insufficiently lowered the pressure to 140-160/80-100 mmHg, so we performed PTRA. Stenotic lesion and pressure gradient was still present after balloon angioplasty on both sides, prompting us to place LUMINEXX® stents on both renal arteries. Blood pressure dropped dramatically after the intervention. Amlodipine was discontinued, and then, enalapril and warfarin were administered to prevent neointima and thrombus formation. Her blood pressure and renal function was stable 18 months after PTRA. Oversized self-expanding stent such as LUMINEXX® stent could be used for renal artery stenting even in pediatric patients with RVH.

Renal artery stenosis

Treatment Atherosclerotic renal artery stenosis It is initially treated with medications, including diuretics, and medications for blood pressure control. When high-grade renal artery stenosis is documented and blood pressure cannot be controlled with medication, or if renal function deteriorates, surgery may be resorted to. The most commonly used procedure is a minimally-invasive angioplasty with or without stenting. It is unclear if this approach yields better results than the use of medications alone. It is a relatively safe procedure. If all else fails and the kidney is thought to be worsening hypertension and revascularization with angioplasty or surgery does not work, then surgical removal of the affected kidney (nephrectomy) may significantly improve high blood pressure. Fibromuscular dysplasia Angioplasty with or without stenting is the best option for the treatment of renal artery stenosis due to fibromuscular dysplasia. See also Renovascular hypertension References

Hypertension

Secondary hypertension Secondary hypertension is hypertension due to an identifiable cause, and may result in certain specific additional signs and symptoms. For example, as well as causing high blood pressure, Cushing's syndrome frequently causes truncal obesity, glucose intolerance, moon face, a hump of fat behind the neck and shoulders (referred to as a buffalo hump), and purple abdominal stretch marks. Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis (RAS) may be associated with a localized abdominal bruit to the left or right of the midline (unilateral RAS), or in both locations (bilateral RAS). Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.

[Natural history of arterial hypertension due to primary hyperreninism].

This case report deals with an eight-year duration severe high renin hypertension and its consequences. In 1975, a 13 years old girl was found to have blood pressure (BP) levels of 240/150 mmHg with bilateral papilloedema. Hypokalemic alkalosis, a 45 mm Sokolow index (SI) and very high peripheral renin activity (PRA) were also noticed. Renal vein renin sampling (RVRS) suggested secretion from the left kidney but intravenous pyelography and renal arteriography were normal. BP levels were first controlled by triple treatment but rose one year later, despite adjunction of beta-blockers. High PRA was again found, but without hormonal gradient on a second RVRS. From 1977 to 1982, BP never fell to normal levels despite quadruple treatment. In 1982, a stage II optic fundus, a 58 mm SI and 2 g/day proteinuria are noticed, so that a new complete etiologic work up is undertaken in 1983: PRA is still high, with a dramatic acute BP fall after captopril and no gradient on a third RVRS, but intravenous pyelography, tomodensitometry and selective arteriography disclose a 4 cm diameter poorly vascularized tumour on the surface of the lower pole of the right kidney. BP levels are controlled for three months by captopril + chlorothiazide. The tumour is removed in january 1984. RVRS by direct peroperative punction indicates (a posteriori) hormonal secretion from the right kidney lower pole. Histologic examination and immunofluorescence with antirenin serum corroborate the juxtaglomerular origin of the tumour. Eighteen months later, BP is permanently normal, SI is 30 mm, and there is no proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Double-blind, parallel, comparative study on quality of life during treatment with amlodipine or enalapril in mild or moderate hypertensive patients: a multicentre study.

To compare tolerance, antihypertensive efficacy and impact on quality of life of amlodipine and enalapril in patients with mild or moderate hypertension. Multicentre, double-blind, double-dummy, comparative trial in general practice. Three phases were conducted: 4 weeks on placebo, 12 weeks of dose adjustment (amlodipine or enalapril) and a 38-week maintenance period. Four hundred and sixty-one patients of both sexes were enrolled; 451 were available for efficacy evaluation at the end of the trial. The patients were allocated to either amlodipine (231) or enalapril (230) treatment. If at the end of dose adjustment (amlodipine 5-10 mg/day, enalapril 10-40 mg/day) diastolic blood pressure was > or = 95 mmHg, hydrochlorothiazide (25-50 mg/day) was added (27 amlodipine patients and 45 enalapril patients). Blood pressure changes after 1 year of treatment; between- and within-group changes in quality of life as assessed by psychological general well-being, social and sexual functioning, health-risk perception, alertness, behaviour, and impact of symptom and side effects. Indices on quality of life were unchanged or increased (2-9%) in both groups. Blood pressure was normalized or reduced by > or = 10 mmHg in 204 (90%) and 190 (85%) patients on amlodipine and enalapril, respectively. Cough was the most frequently reported adverse event in the enalapril group (13%) and oedema in the amlodipine group (22%). Only eight (4%) patients on amlodipine and nine (4%) on enalapril were withdrawn because of drug-related adverse events. At similar blood pressure reduction in mild and moderate hypertension, quality of life is equally well maintained on amlodipine and enalapril therapy.

[Treatment procedures in the vasoconstrictive form of hypertension using calcium antagonists in relation to their effect on kidney function].

Single sublingual administration of nifedipine at a dose of 20 mg to patients with essential hypertension (EH) with subsequent hemodynamic observation every hour for 4 h resulted in the reduction of systolic and diastolic arterial pressure (AP) by 10-15%, arteriolar tone (AT) by 30-40%. Renal metabolism was assessed by the presence of slow isoenzymes of carbonic esterases in urine. They were absent in healthy persons; before nifedipine administration they were detected in 62% of cases, after it--in 22%. Regular administration of nifedipine (30-60 mg/day) and verapamil (160-240 mg/day) in a less severe course of EH (AT less than 4500 conv. units) improved the renal blood flow decreasing AT and AP. Severe EH (AT greater than 4500 conv. units) was characterized by cases of inadequate action of the drugs: dramatic reduction of ERF was followed by a rise of AT and AP which could be accounted for by excessive vasodilation at the 1st stage with further development of the renal steal syndrome and a rise of AP and AT. In such cases lower doses of nifedipine, the combination of verapamil with hydrochlorthiazide and verapamil with prazosin hydrochloride were more effective; the combination of nifedipine with propranolol did not prevent a negative effect on the kidneys and was ineffective in high AT.

Angioplasty

Based on the BASIL trial, the ACCF/AHA guidelines recommend balloon angioplasty only for patients with a life expectancy of 2 years or less or those who do not have an autogenous vein available. For patients with a life expectancy greater than 2 of years life, or who have an autogenous vein, a bypass surgery could be performed first. Renal artery angioplasty Renal artery stenosis is associated with hypertension and loss of renal function. Atherosclerotic obstruction of the renal artery can be treated with angioplasty with or without stenting of the renal artery. There is a weak recommendation for renal artery angioplasty in patients with renal artery stenosis and flash edema or congestive heart failure. Carotid angioplasty

Diagnosis of primary aldosteronism in a patient with an incidentally found adrenal mass.

A 50-year-old woman who was complaining of abdominal pain was referred to the endocrine clinic after a small (0.8 cm by 0.8 cm) mass was found in her right adrenal gland on CT examination of the abdomen. She had a history of hypertension for 10 years, generalized anxiety disorder for 5 years and a weight increase of 18 kg over the previous 3 years. The patient did not report weakness, polyuria or excessive thirst. She had a history of hypokalemia while on hydrochlorothiazide therapy. To improve blood pressure control, a total of three antihypertensive medications had been sequentially added to her regimen. At presentation, medications included 300 mg irbesartan daily, 5 mg amlodipine daily and 100 mg sustained-release metoprolol daily. Renin activity, levels of plasma aldosterone and levels of fractionated plasma metanephrines were measured and an overnight 1 mg dexamethasone suppression test was performed. In addition, measurements of urine aldosterone excretion on a high-salt diet, MRI-examination of the adrenal glands and bilateral adrenal vein sampling were conducted. An aldosterone-secreting adrenal adenoma. The patient underwent laparoscopic resection of the right adrenal gland, which led to normalization of aldosterone excretion, lowering of her blood pressure on a single antihypertensive medication (50 mg sustained-release metoprolol daily) and resolution of hypokalemia.

Kidney ischemia

Renovascular hypertension Renovascular hypertension or renal artery stenosis is characterized as an increase in blood pressure through the arteries to the kidneys. This is due to an abnormal narrowing of the arteries. Acute Renal Failure caused by the treatment of hypertension In patients with hypertension, treatment of the disease using Angiotensin-converting enzyme inhibitors (ACEIs) are sometimes necessary. The glomerular filtration rate(GFR) in patients is regulated by vasoconstriction of the efferent arteriole. When ACEI is taken by the patient, this vasoconstrictor effect of the efferent arteriole is blocked. This then leads to a decrease in GFR and leads to acute renal failure. Studies have shown that 6-38% of patients with renal vascular disease or hypertension will develop acute renal ischemia through acute renal failure.


Patient presenting with fever+tachypnea+FC>100 = 3 criteria of SIRS (Systemic Inflammatory Response Syndrome). Reminder: sepsis is a SIRS due to infection, which leads to a decrease in SVR, resulting in a decrease in preload and stroke volume leading to hypotension. The first therapeutic measures are the administration of empirical broad-spectrum antibiotics and fluid replacement (answer 4) to try to compensate for this decrease in preload. Of choice, balanced crystalloids and albumin solutions [1] But when this is insufficient, we must try to correct the decrease in PVR by using vasoactive drugs [2]. But the vasoactive drug of choice in the context of septic shock is noradrenaline ([3], [4]) (answer 1 FALSE) A minimum of two blood cultures is mandatory (answer 3), for the diagnosis of bacteremia and facilitating a targeted antibiotic treatment. [2] On the other hand, it is interesting to determine blood lactic acid levels for two purposes: it is currently considered the best marker of tissue hypoperfusion/hypoxia and it predicts the response to treatment[2] (answer 2).

Patient presenting with fever+tachypnea+FC>100 = 3 criteria of SIRS (Systemic Inflammatory Response Syndrome). Reminder: sepsis is a SIRS due to infection, which leads to a decrease in SVR, resulting in a decrease in preload and stroke volume leading to hypotension. The first therapeutic measures are the administration of empirical broad-spectrum antibiotics and fluid replacement ([HIDDEN]) to try to compensate for this decrease in preload. Of choice, balanced crystalloids and albumin solutions [1] But when this is insufficient, we must try to correct the decrease in PVR by using vasoactive drugs [2]. But the vasoactive drug of choice in the context of septic shock is noradrenaline ([3], [4]) ([HIDDEN]) A minimum of two blood cultures is mandatory ([HIDDEN]), for the diagnosis of bacteremia and facilitating a targeted antibiotic treatment. [2] On the other hand, it is interesting to determine blood lactic acid levels for two purposes: it is currently considered the best marker of tissue hypoperfusion/hypoxia and it predicts the response to treatment[2] ([HIDDEN]).

A 67-year-old woman with a history of dyslipidemia, who comes to the ED with dysuria and pollakiuria followed by fever, chills, and deterioration of general condition. On arrival she appears severe and is tachycardic, tachypneic, with blood pressure 60/40 mmHg and temperature of 39°C. Which of the following measures would NOT be included in the INITIAL management?

Sepsis, severe sepsis, and septic shock: current evidence for emergency department management.

In the middle of a busy shift, a patient arrives by ambulance from a local long-term care facility with a report of altered mental status. You enter the room to find a chronically ill-appearing 85-year-old man with fever, tachycardia, and hypotension, and it is instantly apparent that this patient is septic. What is not clear is what the source is, what modifications in treatment might be necessary based on preexisting microbial resistance, and which of the array of invasive resuscitation techniques are appropriate when meaningful recovery is questionable and efforts may not be desired by the patient and family. You order IV fluids and broad-spectrum antibiotics; send lab tests, including lactate and cultures of blood, urine, and sputum; and begin to review his extensive history to discuss goals of care with his family and primary doctor. While reviewing these issues, a 54-year-old woman with a history of asthma is brought straight back from triage with respiratory distress. You listen to her lungs, expecting wheezes, but hear decreased lung sounds at the right base, preserved air movement elsewhere, and her skin radiates heat. Now, on the monitor, she has a heart rate of 135 beats per minute, blood pressure of 90/60 mm Hg, O2 saturation of 86%, and a temperature of 39.4 degrees C (103 degrees F). You again identify sepsis and instruct your team that you will be using your department's severe sepsis protocol. Equipment for monitoring and procedures is assembled, your staff provides preprinted order and monitoring flow sheets, and the ICU is alerted. Within an hour, the patient is intubated, has a central line placed, and has received IV fluids, broad-spectrum antibiotics and norepinephrine, and you are pleased to see a MAP of 67 mm Hg, a lactate decreasing from an initial value of 7.0, CVP of 10, and ScvO2 of 78%.

InternalMed_Harrison

Bacteremia Presence of bacteria in blood, as evidenced by positive blood cultures Signs of possibly harmful systemic Two or more of the following condi response tions: (1) fever (oral temperature >38°C [>100.4°F]) or hypothermia (<36°C [<96.8°F]); (2) tachypnea (>24 breaths/min); (3) tachycardia (heart rate >90 beats/min); (4) leukocytosis (>12,000/μL), leukopenia (<4000/μL), or >10% bands Sepsis (or severe sepsis) The harmful host response to infection; systemic response to proven or suspected infection plus some degree of organ hypofunction, i.e.: 1. Cardiovascular: Arterial systolic blood pressure ≤90 mmHg or mean arterial pressure ≤70 mmHg that responds to administration of IV fluid 2. Renal: Urine output <0.5 mL/kg per hour for 1 h despite adequate fluid resuscitation 3. Respiratory: PaO2/FIO2 ≤250 or, if the lung is the only dysfunctional organ, ≤200 4.

Obstentrics_Williams

One scheme for management of acute pyelonephritis is shown in Table 53-2. Urine cultures are taken, but prospective trials show that blood cultures are of limited clinical utility (Gomi, 2015; Wing, 2000). We obtain blood cultures if the temperature is >39°C. Intravenous hydration to ensure adequate urinay ouput is the cornerstone of treatment. Antimicrobials are also begun promptly with the caveat that they may initially worsen endotoxemia from bacterial lysis. Surveillance for worsening sepsis syndrome includes serial monitoring of urinary output, blood pressure, pulse, temperature, and oxygen saturation. High fevers are lowered with a cooling blanket and acetaminophen. his is especially important in early pregnancy because of possible teratogenic efects from hyperthermia.

Surgery_Schwartz

tachycardic, but they do not exhibit a reduction in blood pressure until over 1500 mL of blood loss, or class III shock. Physical findings should be used as an aid in the evaluation of the patient’s response to treatment. The goal of fluid resuscitation is to re-establish tissue perfusion. Fluid resuscitation usually begins with isotonic crystalloid, typically Ringer’s lactate. However, for patients arriving in shock (persistent SBP <90 mmHg in an adult), instead of crystalloid the current practice is to activate a massive trans-fusion protocol (MTP) in which red blood cells (RBC) and fresh frozen plasma (FFP) are administered. The details of a MTP are discussed later. Patients who have a good response to Brunicardi_Ch07_p0183-p0250.indd 19110/12/18 6:17 PM 192BASIC CONSIDERATIONSPART Ifluid infusion (i.e., normalization of vital signs, clearing of the sensorium) and evidence of good peripheral perfusion (warm extremities with normal capillary refill) are presumed to have adequate

First_Aid_Step2

■Signs and symptoms are similar to those of cystitis but show evidence of upper urinary tract disease. ■ Symptoms include f ank pain, fever/chills, and nausea/vomiting. Dysuria, frequency, and urgency are also possible. ■UA and culture: Results are similar to those of cystitis, but with WBC casts. Send blood cultures to rule out urosepsis. Pyelonephritis is the most common serious medical complication of pregnancy. Twenty to thirty percent of patients with untreated bacteriuria will develop pyelonephritis. When in doubt, admit a patient with pyelonephritis and administer IV antibiotics. Urosepsis must be considered in any elderly patient with altered mental status. SIRS = two or more of the following: 1. Temperature: Either < 36°C or > 38°C (i.e., hypothermia or fever). 2. Tachypnea: > 20 breaths per minute or PaCO2 < 32 mmHg on ABG. 3. Tachycardia: HR > 90 bpm. 4. Leukocytosis/leukopenia: WBC < 4000 cells/mm3 or > 12,000 cells/mm3. CBC: Reveals leukocytosis.

Rapidly progressive fatal pneumococcal sepsis in adults: a report of two cases.

We report two cases of a rapidly progressive fatal overwhelming pneumococcal infection. Patient 1 was a 67-year-old man with a 24-h history of fever and malaise and was transferred to our department. He was severely ill, tachypneic, and felt a chill. A purpuric discoloration with ecchymosis of the skin was noted over the body. The chest X-ray findings demonstrated thickening of the bronchovascular bundle in the right lower lung field, which later revealed the presence of bronchopneumonia. Laboratory studies revealed the presence of metabolic acidosis and disseminated intravascular coagulation. After presentation, rapid deterioration occurred followed by cardiopulmonary arrest. Despite cardiopulmonary resuscitation, the patient died only 3 h after presentation. The isolates from the patient's blood revealed penicillin-susceptible Streptococcus pneumoniae, serotype 4. Patient 2 was a 30-year-old woman with a prior history of uneventful pregnancies was transferred to our department with a 2-day history of fever, nausea, headache, and malaise. Although she was in the 19th week of pregnancy at the time, she suffered a miscarriage just prior to admission. Upon presentation to our department, she demonstrated unstable vital signs, diminished consciousness, anuria, and icterus. Purpuric discoloration with ecchymosis of the skin was noted in over most of her body, including the distal extremities. The chest X-ray findings were close to normal. Initial laboratory studies revealed the presence of severe metabolic acidosis and disseminated intravascular coagulation with multiple organ failure. Despite aggressive cardiopulmonary support, normal neurological responses disappeared on the 2nd day following admission and the patient died on the 16th day after admission. The patient's isolates from blood and vaginal swabs both later revealed penicillin-susceptible Streptococcus pneumoniae, serotype 12F. The presentation of rapidly progressive septic shock should raise the treating physician's suspicion of overwhelming pneumococcal infection, which has limited management options.

Who needs a blood culture? A prospectively derived and validated prediction rule.

The study objective was to derive and validate a clinical decision rule for obtaining blood cultures in Emergency Department (ED) patients with suspected infection. This was a prospective, observational cohort study of consecutive adult ED patients with blood cultures obtained. The study ran from February 1, 2000 through February 1, 2001. Patients were randomly assigned to derivation (2/3) or validation (1/3) sets. The outcome was "true bacteremia." Features of the history, co-morbid illness, physical examination, and laboratory testing were used to create a clinical decision rule. Among 3901 patients, 3730 (96%) were enrolled with 305 (8.2%) episodes of true bacteremia. A decision rule was created with "major criteria" defined as: temperature > 39.5 degrees C (103.0 degrees F), indwelling vascular catheter, or clinical suspicion of endocarditis. "Minor criteria" were: temperature 38.3-39.4 degrees C (101-102.9 degrees F), age > 65 years, chills, vomiting, hypotension (systolic blood pressure < 90 mm Hg), neutrophil% > 80, white blood cell count > 18 k, bands > 5%, platelets < 150 k, and creatinine > 2.0. A blood culture is indicated by the rule if at least one major criterion or two minor criteria are present. Otherwise, patients are classified as "low risk" and cultures may be omitted. Only 4 (0.6%) low-risk patients in the derivation set and 3 (0.9%) low-risk patients in the validation set had positive cultures. The sensitivity was 98% (95% confidence interval [CI] 96-100%) (derivation) and 97% (95% CI 94-100%) (validation). We developed and validated a promising clinical decision rule for predicting bacteremia in patients with suspected infection.

Sepsis

Early recognition and focused management may improve the outcomes in sepsis. Current professional recommendations include a number of actions ("bundles") to be followed as soon as possible after diagnosis. Within the first three hours, someone with sepsis should have received antibiotics and, intravenous fluids if there is evidence of either low blood pressure or other evidence for inadequate blood supply to organs (as evidenced by a raised level of lactate); blood cultures also should be obtained within this time period. After six hours the blood pressure should be adequate, close monitoring of blood pressure and blood supply to organs should be in place, and the lactate should be measured again if initially it was raised. A related bundle, the "Sepsis Six", is in widespread use in the United Kingdom; this requires the administration of antibiotics within an hour of recognition, blood cultures, lactate, and hemoglobin determination, urine output monitoring, high-flow oxygen, and

InternalMed_Harrison

The disposition of younger, previously healthy heat-exhaustion patients who have no major laboratory abnormalities may include hospital observation and discharge after IV rehydration. Older patients with comorbidities (including cardiovascular disease) or predisposing factors often require inpatient fluid and electrolyte replacement, monitoring, and reassessment. The clinical manifestations of heatstroke reflect a total loss of thermo-regulatory function. Typical vital-sign abnormalities include tachypnea, various tachycardias, hypotension, and a widened pulse pressure. Although there is no single specific diagnostic test, the historical and physical triad of exposure to a heat stress, CNS dysfunction, and a core temperature >40.5°C helps establish the preliminary diagnosis.

Near-infrared Spectroscopy in Transport With a Patient in Multi-factorial Shock.

A 14-year-old male with a history of repaired truncus arteriosus presented to an outside hospital emergency room in respiratory distress. The triage report to the transport referral center included the following vital signs: temperature of 36.6°C, respiratory rate (RR) of 26 breaths/min, heart rate (HR) of 144 beats/min, and blood pressure (BP) of 113/52 mm Hg with peripheral capillary oxygen saturation (SpO<sub2</sub) of 95% on 4 L via an OxyMask (SouthMedic, Barrie, Ontario, Canada). Additional information indicated severe right ventricle to pulmonary artery conduit stenosis; anuria for 2 days; and cool, mottled extremities. The transport team was dispatched via helicopter. The vital signs upon arrival were as follows: temperature of 36.5°C, HR of 153 beats/min, RR of 48 breaths/min, BP of 81/52, mean arterial pressure of 62, and SpO<sub2</sub of 96% on 8 L via an OxyMask. Physical assessment revealed the patient was alert and oriented, tachypneic, tachycardic, and displaying poor perfusion. An epinephrine drip was initiated while the patient was being prepared for transport. Near-infrared spectroscopy (NIRS) was initiated with cerebral NIRS of 71% and renal NIRS of 39%. The epinephrine drip was escalated, and norepinephrine was initiated and titrated up for continued poor perfusion and low renal NIRS. Vitals at the transfer of care at the receiving facility were HR of 142 beats/min, BP of 91/51 mm Hg, RR of 56 breaths/min, SpO<sub2</sub of 99%, and cerebral NIRS of 75% and renal NIRS of 53%. The patient required mechanical circulatory support shortly after admission. NIRS monitoring was used to help measure perfusion and reassess interventions made during transport.

Risk factors for heat related death during the August 2003 heat wave in Paris, France, in patients evaluated at the emergency department of the Hôpital Européen Georges Pompidou.

This study sought to determine the risk factors for short term mortality in the victims of the heat wave of August 2003 in France from among patients evaluated in our emergency department (ED). It was hypothesised that age, temperature, and some long term therapies and pre-existing pathologies were factors associated with short term mortality. A retrospective analysis of a seven day period. Four experts decided blindly, in pairs, whether a patient had presented with a heat related problem. Inclusion criteria were: core temperature > or =38 degrees C and/or clinical signs of dehydration. Comparisons were made between the survivors and one month non-survivors for 57 different items. Short term mortality was defined as death in the ED or within the first month of the ED visit. Of 841 patients attending the ED in the study period, 165 were included in the study, of which most were elderly women. Thirty one (18.8%) died within one month. Factors associated with short term mortality were: a greater degree of dependent living; more severe clinical condition on admission (higher temperature and heart rate, lower blood pressure, hypoxia, and altered mental status); higher values of blood glucose, troponin, and white blood cell count; lower values of serum protein and prothrombin levels; pre-existing ischaemic cardiomyopathy; pneumonia as associated infection; and previous psychotropic treatment. The total number of survivors at one year was 91. Although this study is limited because of the small sample size, the results have helped determine factors useful for future identification of patients at greatest risk of death in order to implement a more efficient patient care protocol.

[Status epilepticus induced by prolonged immersion in hot herb bath: report of one case].

A 6-year-old girl with cerebral palsy developed conscious disturbance and generalized convulsion after one-hour hot herb drug bath. Physical examination on admission revealed rectal temperature 41 degrees C, hot skin, respiration 46/min, regular heart beat 98/min, BP 130/60 mmHg, Glascow coma scale 4 (E2M1V1), soft and flat abdomen, no hepatosplenomegaly, no skin rash, no focal neurological sign, increased generalized muscle ton. Laboratory data showed CBC: WBC 20400 cumm (Neutrophils 31%, Lymphocytes 69%), Hb 11.6gm%, ESR 11 mm/hr, arterial blood gas: PH 7.077, PO2 43mmHg, PCO2 57.1mmHg, HCO3- 16 mEq/L, BE-11.5mEq/L, serum sodium 143 mEq./L, potassium 5.2 mEq/L, chloride 101 mEq/L, free calcium ion 3.8mg%, GOT 63IU/L, GPT 263 IU/L, amylase 193 IU/L, alkaline phosphatase 388 IU/L, LDH 1245 IU/L, CPK 677 IU/L, total bilirubin 0.8 mg/dl, direct type 0.1 mg/dl, BUN 18 mg/dl, Glucose 35 mg/dl. Urinalysis revealed proteinuria( ) trace hematuria and pyuria, but no cast. Lumbar puncture is within normal limits. Bacteriology including blood and CSF are normal. Multiple organ failure was noted at that time. Intensive cooling methods were performed including central and peripheral cooling. We used luminal and valium to control the seizure. Condition didn't improve. Afterwards cardiopulmonary arrest developed. Patient expired 8 hours after admission despite of resuscitation. Heat stroke in infancy and childhood is different from that in adulthood. The predisposing factors are high ambient temperature, dehydration, very young baby, sweat gland dysfunction, or ectodermal dysplasia. Definition of heat stroke includes 1) rectal temperature above 41 degrees C, 2) behavioral change, 3) warm skin, wet or dry.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypotension

Volume resuscitation (usually with crystalloid or blood products) Blood pressure support with a vasopressor (all seem equivalent with respect to risk of death, with norepinephrine possibly better than dopamine). Trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults. Ensure adequate tissue perfusion (maintain SvO2 >70 with use of blood or dobutamine) Address the underlying problem (i.e., antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...) The best way to determine if a person will benefit from fluids is by doing a passive leg raise followed by measuring the output from the heart.

[Electrocardiographic and hemodynamic changes during systemic hyperthermia (42 degrees C)].

During systemic hyperthermia (42 degrees C), depression of ST segments or T wave changes in the left precordial leads were noticed in 56% of patients, and 29% of cases showed right bundle branch block. Supraventricular tachycardia was found in 26% and temporary deviation of mean frontal vector to the left axis was observed in 15%. These changes disappeared following recovery to normal temperature. The ECG findings for any particular patient were similar even during a second period of hyperthermia. Pulse rate became elevated by 1.7 times, and cardiac output became up to 2.4 times higher at 42 degrees C.

A Middle-Aged Woman With Hematochezia, Hypotension, and Leg Cramps.

A 57-year-old woman with a history of mantle cell lymphoma presented to the ED with complaints of vomiting, bleeding per rectum, and leg cramps, that started 6 h prior to her arrival. She had received chemotherapy a week prior. Her leg cramps were not associated with pain or swelling of the legs; she also denied any trauma to the legs. She did complain of mild lower abdominal pain at presentation. Review of systems was negative for fever, chills, diarrhea, chest pain, and dizziness. She denied using alcohol or nonsteroidal anti-inflammatory drugs. The patient was tachycardic with a systolic BP (SBP) of 85 mm Hg and was administered 1-L normal saline, with improvement in her SBP to 90 mm Hg. The hematocrit level was 24%, the WBC count was 0.3 × 10<sup9</sup/L, and the platelet count was 6 × 10<sup9</sup/L in the ED. On arrival in the ICU, she was noted to have an SBP of 70 mm Hg. Resuscitation with IV fluids was initiated, followed by transfusion of packed RBCs and platelets, based on the blood counts. Despite aggressive fluid resuscitation and improvement in her hemoglobin, the patient remained persistently hypotensive. The diagnosis of underlying septic shock because of neutropenia was considered; the patient was started on vasopressors and empirical broad-spectrum antibiotics, with improvement in her BP. After this, the patient was sent to radiology for a CT scan of the abdomen and pelvis with contrast to evaluate for mesenteric infarction, enteric or colonic bleeding, and the need for arterial embolization.

Cases from the Osler Medical Service at Johns Hopkins University.

PRESENTING FEATURES: A 70-year-old African American man was admitted with a history of fever, chills, and malaise of several days' duration. His past medical history was notable for end-stage renal disease requiring hemodialysis, coronary artery disease, and aortic stenosis requiring a bioprosthetic aortic valve replacement. On the day of admission, the patient was noted to have a shaking chill while undergoing dialysis through his catheter and was admitted to the hospital. He complained of pain at the catheter insertion site, shortness of breath, and dyspnea on exertion, but denied chest pain. On physical examination, the patient had a temperature of 100.4 degrees F, with a heart rate of 64 beats per minute, blood pressure of 127/72 mm Hg, and an oxygen saturation of 97% on room air. He was a mildly obese man in no apparent distress. He had shotty cervical lymphadenopathy and a right subclavian dialysis catheter in place, with erythema and pus at the entry site. His jugular venous pressure was 10 cm H(2)O. Lung examination showed bibasilar rales. Heart sounds were normal, with no rub or gallop. He had a 2/6 systolic ejection murmur best heart at the left sternal border as well as a 3/6 holosystolic murmur at the apex that radiated to his left axilla. Examination of the abdomen and extremities was unremarkable. The patient's neurological examination was unremarkable, and he was alert and oriented to person, place, and time. Laboratory studies showed an elevated white blood cell count of 16,700 cells/microL. His blood urea nitrogen level was 43 mg/dL and his serum creatinine level was 4.9 mg/dL. Multiple blood cultures grew methicillin-resistant Staphylococcus aureus. An admission, chest radiograph showed no infiltrate. An admission electrocardiogram showed normal sinus rhythm with first degree atrioventricular block, left anterior fascicular block, and left ventricular hypertrophy. shows rhythm strips from lead II electrocardiograms 5 months before admission (top), on admission (middle) and 5 days after admission (bottom). What is the diagnosis?

A middle-aged female with recurrent sinopulmonary infections: a case report.

Common variable immunodeficiency (CVID) is a form of severe antibody deficiency with an estimated prevalence of 1 in 25,000 to 1 in 100,000. The disorder apparently results from currently undefined immune deregulations resulting in failed B-cell differentiation with impaired secretion of immunoglobulins. It has a broad range of clinical symptoms including recurrent infections of the respiratory tract, chronic lung disease, autoimmune diseases, liver and gastrointestinal disorders, granulomatous infiltrations, lymphoma and solid tumors. A 42-year-old Caucasian female presented with a one-day history of high-grade fever and productive cough associated with retrosternal chest pain. The patient had been discharged one week prior after a prolonged stay in an intensive care unit with multiorgan failure requiring temporary hemodialysis for two weeks secondary to sepsis. Past medical history was significant for chronic obstructive pulmonary disease, recurrent pneumonias and recurrent sinus infections since adolescence. She had a temperature of 99.8 degrees F, was tachycardic (137/min), tachypneic (26/min) with a blood pressure of 109/59 mmHg and oxygen saturation of 88% on 2 l/min nasal oxygen. Physical examination was significant for bibasilar rhonchi. Laboratory data were significant for leukocytosis of 15,700/mm3. Chest X-ray demonstrated bibasilar infiltrates. The patient was started on intravenous levofloxacin and vancomycin, and sputum gram stain and cultures were performed. Given the patient's recurrent respiratory infections, an underlying immunologic disorder was considered. Work-up revealed immunoglobulin A (IgA) 11 mg/dl (normal 70-400 mg/dl), immunoglobulin M (IgM) 2 mg/dl (normal 40-230 mg/dl) and IgG 53 mg/dl (normal 700-1,600 mg/dl). The patient was diagnosed with CVID and started on intravenous immunoglobulin. She was initially started on a four-week regimen of intravenous immunoglobulin, which was later switched to a three-week regimen as the patient had respiratory infections on the four-week regimen. She remained asymptomatic on a three times/week intravenous immunoglobulin regimen. This case emphasizes the need for a high index of clinical suspicion for CVID in patients presenting with recurrent sinopulmonary infections. Although intravenous immunoglobulin provides improvement in these patients, early diagnosis is the key to preventing significant morbidity and mortality and improving prognosis.

[Factor analysis fever in the early postoperative period following cardiopulmonary bypass surgery in adults. Correlation with bacteriological data. Statistical study of 518 case histories by computer].

The results of a continuous series of 518 adults undergoing cardiopulmonary bypass surgery, operated on by the same surgeon, comprising valvular replacement and aorto-coronary bypass surgery with a peroperative protocol of asepsis and a short prophylactic course of Penicillin and Streptomycin, a preoperative and postoperative bacteriological study, were treated by computer. The postoperative temperature chart showed a progressively decreasing pyrexia in the first 8 days after cardiopulmonary bypass. The nature of the operation, the bypass time, the quantity of blood used during operation and the blood loss were statistically significant factors. Patients with a clinical infection had significantly higher temperatures from the first on. 8,9% of patients had a febrile reaction which continued after the 10th day after cardiopulmonary bypass. The cause was not always apparent but the appearance of their temperature graphs was distinguishable after the first week. Analysis of the systematic bacterial specimens showed bacterial contamination of nearly 10% of drains, 10% of blood cultures, over 15% of intravenous infusion catheters and 70% of urinary catheters. The significance of these results is discussed. The normal appearance of the temperature chart after cardiopulmonary bypass surgery in the absence of clinical complications and bacterial contamination has been established.

[Autoimmune hepatitis complicated by intolerable pain of lower extremities and shock due to azathioprine].

A 24-year-old woman was followed for about ten months with oral administration of prednisolone (22.5-35 mg/d) for autoimmune hepatitis. In June 1995, she noticed fatigue and appetite loss and blood chemistry revealed markedly deteriorated liver function. She was admitted to our hospital. The daily dose of prednisolone was increased to 60 mg. Her elevated levels of transaminases decreased gradually. Administration of azathioprine (100 mg/d) was started with tapering of prednisolone on August 18th. Ten days later, tender cervical lymphadenopathy and high fever occurred. Azathioprine administration was stopped immediately and intravenous antibiotics were given. On September 5th, 50 mg of azathioprine was administered again. Two hours later, the patient complained of intolerable pain from the lumbar region to the knee joints, which subsided following two injections of analgesics within a few hours. However, chills, high fever and hypotension (86/30 mmHg) subsequently developed. No bacterial growth was detected in blood culture. She was discharged on September 12th. On October 4th, she visited our out-patient clinic. The next day, she took one tablet (50 mg) of azathioprine at 10 o'clock. She noted intense pain from the thighs to the knees and calves around noon again. Her home doctor found that she exhibited shock (BP 67/?). She was immediately taken to our department. The same symptoms and signs as the above-mentioned occurred. Azathioprine was considered responsible for these two adverse reactions (shock) as an allergen. Later, systemic lupus eythematosus was diagnosed in 1996. And she died to pulmonary hypertension in May 1999. Physicians should be aware of the potential adverse effect of azathioprine administered in order to manage the patients with autoimmune disorders.

[Influence of axillary temperature on blood culture yield in the emergency department].

To determine the clinical and epidemiological characteristics of patients undergoing blood culture in the emergency department and to identify the relation between the results of blood culture and axillary temperature at blood extraction. We performed a prospective, observational study. All patients who underwent blood extraction by 2 emergency department nurses, as indicated by physicians, between January 2004 and December 2005 were included. The patients were stratified into subgroups according to their temperature on extraction and final diagnosis. Bivariate analysis was performed to compare the clinical and epidemiological characteristics of the patients in relation to the presence of bacteremia and the distinct subgroups established. Isolates of common contaminating microorganisms were discarded. A total of 603 patients were included. The highest percentages of bacteremia were found in patients with high fever or hypothermia. Among the overall group of patients, a significant correlation was found between axillary temperature and bacteremia. However, when patients with a final diagnosis of a disease with a low probability of bacteremia were excluded, this correlation disappeared and no association was found between temperature and the risk of bacteremia in specific infectious processes (pneumonia, pyelonephritis, etc). The main factor associated with bacteremia was the disease prompting blood culture rather than patient temperature.

2-Methyl-4-chlorophenoxyacetic acid (MCPA) and bromoxynil herbicide ingestion.

Ingestion of bromoxynil and 2-methyl-4-chlorophenoxyacetic acid (MCPA) in combination is associated with high mortality. Toxicity is characterised by hyperthermia and metabolic acidosis. Dialysis is a proposed treatment, but little data exist regarding its effectiveness. Case 1: A 50-year-old female presented 18 h post-ingestion of 200  mL of bromoxynil(200 g/L) and MCPA(200 g/L). She was agitated, tachycardic and tachypnoeic. She was intubated and continuous venovenous haemodiafiltration (CVVHDF) was commenced. She deteriorated, becoming hypotensive, hyperthermic (39.5 °C) and hypercapnic (80 mmHg). She was cooled, paralysed, received CVVHDF for 2d and was extubated on day 4 making a full recovery. Case 2: A 60-year-old male presented 6 h post-ingestion of an unknown amount of bromoxynil (200 g/L) and MCPA (200 g/L). On arrival, he was tachycardic and tachypneic (pCO<sub2</sub 25 mmHg). At 8h post-ingestion he became hyperthermic, hypercapnic and acidotic (pH 7.15), and was intubated, paralysed, cooled and received CVVHDF for 36 h. He was extubated after 42 h and made a full recovery. Bromoxynil and MCPA serum and effluent concentrations were measured. Peak MCPA serum concentrations were 161 µg/ml and 259 µg/ml and peak bromoxynil concentrations were 119 µg/ml and 155 µg/ml in case 1 and 2, respectively. The estimated clearance of both herbicides by CVVHDF was low (<10 mL/min). CVVHDF did not result in significant clearance of either herbicide but may have assisted with hyperthermia control. Both patients survived with vigorous cooling, paralysis and ventilatory support.

[Blood cultures when fever?].

A 78-year-old man was referred from his residency where he lives to the emergency division due to general deterioration and frequent falls in the last week. His personal history is remarkable for arterial hypertension and diabetes. Two weeks before he needed a vesical catheterism that was traumatic and profilactic ciprofloxacin was prescribed. On physical exploration he appears disoriented, blood pressure is 9/40 mm Hg, cardiac rythm 120 beats per minute, temperature 37,3 °C and 24 respirations per minute. He appears to have pain on his upper left abdomen cuadrant. When the nurse gets a peripheral vein she asks, ¿should I obtain hemocultures?

Major trauma

A FAST exam may help assess for internal bleeding. In certain traumas, such as maxillofacial trauma, it may be beneficial to have a highly trained health care provider available to maintain airway, breathing, and circulation. Intravenous fluids Traditionally, high-volume intravenous fluids were given to people who had poor perfusion due to trauma. This is still appropriate in cases with isolated extremity trauma, thermal trauma, or head injuries. In general, however, giving lots of fluids appears to increase the risk of death. Current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries, allowing mild hypotension to persist. Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, or the re-establishment of peripheral pulses and adequate ability to think. Hypertonic saline has been studied and found to be of little difference from normal saline.

The Absence of Fever Is Associated With Higher Mortality and Decreased Antibiotic and IV Fluid Administration in Emergency Department Patients With Suspected Septic Shock.

This study evaluates whether emergency department septic shock patients without a fever (reported or measured) receive less IV fluids, have decreased antibiotic administration, and suffer increased in-hospital mortality. This was a secondary analysis of a prospective, observational study of patients with shock. The study was conducted in an urban, academic emergency department. The original study enrolled consecutive adult (aged 18 yr or older) emergency department patients from November 11, 2012, to September 23, 2013, who met one of the following shock criteria: 1) systolic blood pressure less than 90 mm Hg after at least 1L IV fluids, 2) new vasopressor requirement, or 3) systolic blood pressure less than 90 mm Hg and IV fluids held for concern of fluid overload. The current study is limited to patients with septic shock. Patients were grouped as febrile if they had a subjective fever or a measured temperature >100.4°F documented in the emergency department; afebrile patients lacked both. Among 378 patients with septic shock, 207 of 378 (55%; 50-60%) were febrile by history or measurement. Afebrile patients had lower rates of antibiotic administration in the emergency department (81% vs 94%; p < 0.01), lower mean volumes of IV fluids (2,607 vs 3,013 mL; p < 0.01), and higher in-hospital mortality rates (33% vs 11%; p < 0.01). After adjusting for bicarbonate less than 20 mEq/L, lactate concentration, respiratory rate greater than or equal to 24 breaths/min, emergency department antibiotics, and emergency department IV fluids volume, being afebrile remained a significant predictor of in-hospital mortality (odds ratio, 4.3; 95% CI, 2.2-8.2; area under the curve = 0.83). In emergency department patients with septic shock, afebrile patients received lower rates of emergency department antibiotic administration, lower mean IV fluids volume, and suffered higher in-hospital mortality.

A successful management after preterm delivery in a patient with severe sepsis during third-trimester pregnancy.

A 33-year-old woman visited the emergency department presenting with fever and dyspnea. She was pregnant with gestational age of 31 weeks and 6 days. She had dysuria for 7 days, and fever and dyspnea for 1 day. The vital signs were as follows: blood pressure 110/70 mmHg, heart rate 118 beats/minute, respiratory rate 28/minute, body temperature 38.7℃, and oxygen saturation by pulse oximetry 84% during inhalation of 5 liters of oxygen by nasal prongs. Crackles were heard over both lung fields. There were no signs of uterine contractions. Chest X-ray and chest computed tomography scan showed multiple consolidations and air bronchograms in both lungs. According to urinalysis, there was pyuria and microscopic hematuria. She was diagnosed with community-acquired pneumonia and urinary tract infection (UTI) that progressed to severe sepsis and acute respiratory failure. We found extended-spectrum beta-lactamase producing <iEscherichia coli</i in the blood culture and methicillin-resistant Staphylococcus aureus in the sputum culture. The patient was transferred to the intensive care unit with administration of antibiotics and supplementation of high-flow oxygen. On hospital day 2, hypoxemia was aggravated. She underwent endotracheal intubation and mechanical ventilation. After 3 hours, fetal distress was suspected. Under 100% fraction of inspired oxygen, her oxygen partial pressure was 87 mmHg in the arterial blood. She developed acute kidney injury and thrombocytopenia. We diagnosed her with multi-organ failure due to severe sepsis. After an emergent cesarean section, pneumonia, UTI, and other organ failures gradually recovered. The patient and baby were discharged soon thereafter.

EMS Clinical Diagnosis Without The Use Of A Thermometer -- Issues of Concern

The subjective assessment of fever, as well as the assessment of other signs and symptoms that occur with infectious disease, is important in EMS. Pulse can be high due to fever, or with possible associated dehydration or shock. Palpating a pulse not only gives an accurate rate, but it also gives information about the effectiveness of blood pressure and flow. This can be of significant concern with a severe infectious disease, especially sepsis. Shock can develop quickly and differentiating infectious cause for shock will be important for definitive treatment. Unfortunately, people taking medications affecting the heart rate (such as beta blockers or calcium channel blockers) may not mount a tachycardic response, so a normal heart rate does not rule out fever or infection. Additionally, sepsis, especially in the elderly, can actually cause bradycardia (associated with end-organ failure.)

Septic shock

Treatment Treatment primarily consists of the following: Giving intravenous fluids Early antibiotic administration Early goal directed therapy Rapid source identification and control Support of major organ dysfunction Fluids Because lowered blood pressure in septic shock contributes to poor perfusion, fluid resuscitation is an initial treatment to increase blood volume. Patients demonstrating sepsis-induced hypoperfusion should be initially resuscitated with at least 30 ml/kg of intravenous crystalloid within the first three hours. Crystalloids such as normal saline and lactated Ringer's solution are recommended as the initial fluid of choice, while the use of colloid solutions such as hydroxyethyl starch have not shown any advantage or decrease in mortality. When large quantities of fluids are given, administering albumin has shown some benefit.

[Accidental deep hypothermia and circulatory arrest. Treatment with extracorporeal circulation].

A 27-year old female was discovered at 4 a.m. lying in a wet field, the ambient temperature being of 4 degrees C. Her rectal temperature had fallen to 19 degrees C. She was comatose and failed to respond to noxious stimuli. Her pupils were dilated and fixed. Her respiratory rate was reduced to three to four breaths per min. Her blood pressure was not measurable and neither femoral or carotid pulse could be detected. The heart was in sinus rhythm with a rate of 40 b X min-1. During her transfer to hospital, she was ventilated with oxygen, a tidal volume of 300 ml and a rate of 10 b X min-1. On arrival in the emergency room, a short period of ventricular fibrillation preceded cardiac arrest. Cardiac massage and sodium bicarbonate infusion were continued during the transfer of the patient to the operating theatre. A femoro-femoral cardiopulmonary bypass was started with a bloodless priming, 3 mg X kg-1 heparin and a flow of 3,000 to 3,500 ml X min-1. Mean arterial pressure was maintained between 65 and 85 mmHg; cardiac massage was discontinued during the bypass. Within 50 min, ventricular fibrillation appeared, rectal temperature had increased to 33 degrees C. Electrical defibrillation (300 J) was successful. Cardiopulmonary bypass was stopped after 63 min. The postoperative course was uneventful, apart from transient pulmonary oedema. At the time of discharge, a week later, no loss of intellect or change in behaviour could be perceived.(ABSTRACT TRUNCATED AT 250 WORDS)

Shock (circulatory)

of 40 mmHg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified. The pathophysiology behind septic shock is as follows: 1) Systemic leukocyte adhesion to endothelial cells 2) Reduced contractility of the heart 3) Activation of the coagulation pathways, resulting in disseminated intravascular coagulation 4). Increased levels of neutrophils

Mycotic pseudoaneurysm of the brachiocephalic artery.

A 73-year-old woman with a history of hypertension and hyperlipidemia presented with a sharp pain ranging from the right shoulder to the upper limb. She had suffered a sharp pain at rest accompanied by general fatigue and nausea for about ten months prior to admission. Her white blood cell count was 12,800/microl, and her serum C-reactive protein was 17.5 mg/dl. A chest computed tomography scan revealed an aneurysmal change of the origin of the brachiocephalic artery. Pseudoaneurysm due to infection and aortic dissection was considered as a preoperative diagnosis. A total arch replacement was performed under cardiopulmonary bypass, deep hypothermia, and selective cerebral perfusion. Postoperatively, a bacteriologic culture of the contents of the aneurysm revealed Staphylococcus aureus. Perioperative administration of antibiotics was effective and the postoperative course was uneventful.

Sepsis

Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. This initial stage is followed by suppression of the immune system. Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion. There may also be symptoms related to a specific infection, such as a cough with pneumonia, or painful urination with a kidney infection. The very young, old, and people with a weakened immune system may have no symptoms of a specific infection, and the body temperature may be low or normal instead of having a fever. Severe sepsis causes poor organ function or blood flow. The presence of low blood pressure, high blood lactate, or low urine output may suggest poor blood flow. Septic shock is low blood pressure due to sepsis that does not improve after fluid replacement.

[An elder case of accidental hypothermia].

A 87-year-old woman with accidental hypothermia was admitted to our hospital. On admission, she showed consciousness disturbance (JSC III-200) the decorticate rigidity and shock. Her body temperature was too low to been measured and her ECG revealed a J wave. She received the external rewarming and warm fluid replacement. Her consciousness level recovered to JSC II-20 after 2.5 hours of treatment, to JCSI-1 after 7.5 hours. Her body temperature reached 34.5 degrees C 9.5 hours later, and the J wave on ECG disappeared. She was discharged without complications on the 6th hospital day. it was suggested that early diagnosis and the proper therapy improves the mortality of accidental hypothermia.