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العودة   منتديات الحصاحيصا نت alhasahisa > «۩۞۩-المنتديات الخاصة-۩۞۩» > «۩۞۩-منتدى الأسرة والصحة-۩۞۩»

«۩۞۩-منتدى الأسرة والصحة-۩۞۩» كل ما يخص الامور الطبية والصحية

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#1  
قديم 06-22-2012, 11:54 AM
د/منصور غير متواجد حالياً
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افتراضي Clinical Case Discussion









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قديم 06-22-2012, 12:29 PM   #2




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ماشاءالله منتدي الاسرة والصحة ملئ بالمواد العلمية

جزاك الله خير يادكتور ابداع


 
 توقيع : ابوعمر



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قديم 06-22-2012, 04:06 PM   #3


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[quote=ابوعمر;223763]ماشاءالله منتدي الاسرة والصحة ملئ بالمواد العلمية

جزاك الله خير يادكتور ابداع.


مشكور ياحبيب ..ربنا يوفق الجميع ..ونتمنى من الاخوة الاطباء والكوادر الصحية الاخرى أن لايبخلوا علينا بعلمهم،ويساهموا حتى لو بالقليل حتى تعم الفائدة ـــــ وهذه المساحة مفتوحة لجميع الاطباء لمناقشة الحالات المهمة والشائعة من الامراض.



ـ a full term baby boy brought by his mother weighing 3.8 kg. developed jaundice at 2nd day of life
. coomb's test –ve ,Hb : 18 ,billrubin : 18.9 &
indirect: 18.4
O/E : baby was healthy and feeding well .. the most
likely diagnosis is :

a- physiological jaundice
b- ABO incompatibility
c- breast milk jaundice
d- undiscovered neonatal sepsi
s


 
 توقيع : د/منصور



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قديم 06-25-2012, 06:43 PM   #4


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[LEFT]9-Nahed is 45 years old female teacher who presented to ER last night suffering from severe epigastric pain that radiating to back and associated with three blood free vomitus , continuous nausea and pain for the last six hours, pain is severe that she could not stand, there was no fever , no loss of consciousness , past history revealed.
That she did abdominal ultrasound six months ago which revealed gallstone, however she denied any similar attacks in the past No history of past admission or chronic diseases. She looked in pain Temp=37C, Bp=100/60 mmHg, no pallor or jaundice , abdominal examination revealed tender epigastrium. The most likely diagnosis would be:

a-perforaled duodenal ulcer.
b-Rupture abdominal aortic aneurysm
c-Acute pancreatitis
d- Acutc hepatitis
c-Inferior myocardial infarction .
10-Initial investigations that should be asked for Nahed inctude all the following except :
a-Serum Amylase .
b-Abdominal plain-X-rays.
c-Abdominal ultrasound .
d-liver function tcst.
c-Endoscopy.
11- Management of Nahed should include all the following except :
a-Keeping her NPO.
b-Monitoring mnput ad output.
c-Starting IVF
d-Starting IV antibiotics .
e-Replace Ca Mg .
12-Details investigations showed that Aisha had acute pancreatitis, Which one of the following is least likely causeof this condition?
a-High triglyceride .
b-Gallstones.
c-H.pylori
d-Viral infections.
e-Alcoholism.
13 Severity of this condition is assessed by all the following parameter :
except
a-Serum calcium.
b-WBC
c-Blood glucose
d-Amylase .
c-LDH
14-All the following are expected complications of acute pancreatitis except :

a-pleural effusion
b-Mal-absorption
c-psudocyst.
d-DM .
e-pancreatic carcinoma


15-One of the following vitamins is not necessary to be prscribed for patient suffering from chronic pancreatitis :

a-Vit-k
b-Vit-D
c-Vit-C
d-Vit-E
e-Vit-A
16-Saeed is a 67 years old male Presented to your clinic complaining of mild to moderate upper abdominal pain for the last3months weight decreased by seven kilograms since that time.
He suffered from generalized fatigue. He is smoker for the last forty years (20 cigarcties /day), no history of drinking alcohol of chronic diseases or past admission to hospital. He was looked ill, in pain, his weight was 67 kgs, BP=120/70 mmhg, no pallor or jaudice,no clubbing, abdominal examination showed epigastric tenderness and 2*2 palpable mass The least likely diagnosis in this patent would be:
a-Gastric cancer .
b-Liver cancer
c-Colon cancer
d-Irritable bowel syndrome
e-Pancreas caner

17-To rule in or rule out the definite diagnosis the first investigation that should be asked is :
a-A abdominal ultrasound
b-Endoscopy.
c-Barium meal.
d-Colonoscopy.
e-Pancreas cancer .
18-Later on the diagnosis was confirmed by CT scan to be A deno-carcinoma of pancreas Senior surgon asked you about this condition, you could tell him all the following information except:
a-This tumor has poor prognosis
b-Most of patients could be managed by surgical resection of tumor .
c-Chemotherapy and radiotherapy are two options of treatment .
d-pain control in the patents suffering from this problem is the cornerstone of management .
19-Which of the following is established as a risk factor for adenocarcinoma of pancreas ?
a-Alcohol intake
b-Smoking
c-Family history
d-History of gasreatomy
c-White race .







[/LEFT]


 
 توقيع : د/منصور



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قديم 08-26-2012, 11:35 AM   #5


الصورة الرمزية د/منصور
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Male
لوني المفضل : Blueviolet
افتراضي



A 68-year-old woman of Persian descent with a past medical history of diabetes mellitus presents to the emergency department (ED) with substernal chest pressure and progressive dyspnea that has lasted for 4 days. Her symptoms have gradually progressed to the point where she has significant dyspnea even at rest; this prompted her decision to come to the ED. On a couple of occasions, she has had associated palpitations with presyncopal symptoms that required her to stop and rest for several minutes. Her chest pressure has become constant in the last 2 hours. She describes it as moderate in intensity, nonradiating, nonpleuritic, and nonpositional. She is usually a quite active person who walks 1-2 miles per day and works in her garden. She notes that these symptoms have slowed her down to the extent that she has trouble doing basic activities around the house. She has never had symptoms similar to these in the past and she is quite concerned. Further review of her systems reveals no evidence of lower extremity edema, orthopnea, or paroxysmal nocturnal dyspnea. In addition, she denies having any long-distance travel, recent surgery, or immobilization. Her medications include an oral hypoglycemic and an angiotensin-converting enzyme (ACE) inhibitor. Her family history is remarkable for diabetes, but there is no history of early coronary artery disease.

On initial physical examination, the patient is awake, calm, and alert. She is tachypneic and is using some accessory muscles in her breathing. She is afebrile. The patient has a heart rate of 95 bpm and a blood pressure of 138/76 mm Hg. Her respiratory rate is accelerated at 30 breaths/min and she has an oxygen saturation of 82% while breathing room air. Her neck veins are distended at 8-10 cm. Her heart sounds include S1 and S2 sounds, with some irregularity to the rhythm. Her lungs have faint crackles bilaterally. Her extremities are cool but with good distal pulses.

She is immediately provided oxygen by means of a nonrebreather face mask and attached to a cardiac monitor with continuous pulse oximetry. Intravenous access is established and blood is sent to the laboratory. A chest radiograph is arranged. An initial electrocardiogram (ECG) is obtained
- The patient in this case had an interesting set of complaints and presenting physical examination findings. Her history was significant for ischemia and heart failure, which were likely caused by a low cardiac output state. Her presyncope was derived from intermittent hypotension related to episodes of profound bradycardia.


 
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قديم 08-26-2012, 11:37 AM   #6


الصورة الرمزية د/منصور
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افتراضي



On presentation to the ED, her heart rate and blood pressure appeared deceptively normal, despite the evidence of heart failure on the physical examination (ie, elevated neck veins, cool extremities, hypoxemia, and crackles in the lung fields). The ECG revealed how serious her condition was and why there appeared to be a paradox. The patient had Mobitz type II second-degree atrioventricular block, a disease of the conduction system distal to the atrioventricular node that can lead to third-degree atrioventricular block. It is likely that she had intermittent third-degree atrioventricular block, which lead to her low cardiac output symptoms.

Though her heart rate was initially in the nineties, she soon revealed what had been happening to her as the telemetry strips alarmed and she became diaphoretic and lightheaded. She became profoundly bradycardic, with a heart rate of 42 bpm and systolic blood pressures in the eighties. Her rhythm strip (see Figure 2) revealed third-degree atrioventricular block. The P-waves were measured at a rate of 125 bpm. The QRS complex revealed a stable escape rhythm of 42 bpm and was independent of the atrial rhythm. Given its narrow morphology, it likely stemmed from somewhere in the conduction system just below the level of the atrioventricular node. The cardiology service was quickly consulted and the patient was transferred to the cardiac care unit after urgent transvenous pacer placement.

Atrioventricular block is a disturbance in the conduction system that causes transient or permanent impairment of electrical activation from the atria to the ventricles. There are 3 categories of conduction disturbance: first-degree, second-degree, and third-degree atrioventricular block. In first-degree atrioventricular block, the conduction is delayed (a PR interval greater than 200 milliseconds), but all atrial impulses are conducted to the ventricles. In second-degree atrioventricular block, some impulses are conducted, whereas others are not. Second-degree atrioventricular block is further subdivided into 2 types, which are called Mobitz type I and Mobitz type II. In Mobitz type I, there is frequently progressive delay in the conduction time to the ventricles until an impulse is not conducted. This is an often physiologically mediated state on an area higher up in the conduction system of the atrioventricular node. In fact, young children and athletes can often be found to have Mobitz type I as an incidental finding. In Mobitz type II, the area of conduction disease is just below the atrioventricular node. The length of the impulse conduction does not change; however, there is lack of conduction at times. In third-degree atrioventricular block, there is no impulse conduction at any time.[1,2,3]

Her initial ECG was Mobitz type II; it can be differentiated from complete heart block because a P wave preceded every QRS complex, with a constant PR length. This is unlike complete heart block, in which the P waves and QRS complexes are not related. After every fifth impulse, the impulse of the P-wave is not conducted. The ECG pattern differed from Mobitz type I block (Wenckebach pattern) because the PR interval did not change at all. As mentioned, in a Wenckebach pattern, the PR interval progressively lengthens until a QRS complex is dropped. In some cases, when a 2:1 (2 P-waves to 1 QRS complex) block is present, type I and type II second-degree blocks are difficult to distinguish. This is because there is no way to discern whether or not the PR interval is lengthening. In such cases, it is important to assess the QRS morphology; when narrower and more like native QRS complexes, the block is often higher in the conduction system, which is consistent with Mobitz type I. This is not, however, an absolute. As a result, it is also important to take into account the clinical history and carefully review the telemetry for any brief transition from 2:1 to 3:2 conduction block, where PR interval changes can be assessed. Sometimes, the differentiation must be undertaken in the electrophysiology laboratory by making use of atria-His and His-ventricle conduction times. This distinction between a Mobitz type I and Mobitz type II is critical because the latter, as in this case, is considered a high-degree, unstable block with the potential to progress to third-degree or complete heart block.[1,2,3]

Conditions that mimic Mobitz type II must also be considered in the differential diagnosis and ruled out. Two possibilities are nonconducting premature atrial contractions and a physiologic block of atrial tachycardia or flutter. In the first condition, multiple P-waves precede a QRS complex, but the morphologies of the P-waves and the P-P intervals can vary. In the second condition, the physiologic decremental conduction or refractoriness of the atrioventricular node prevents underlying atrial tachycardia from leading to a corresponding ventricular tachycardia. The ventricular rate is likely to be rapid in a physiologic block, which distinguishes it from a Mobitz II block, in which bradycardia is more common. The underlying atrial rates are often >150 bpm.[1,2,3]

In addition to the rhythm, the presumed location of the block also has implications for the patient's care. Conduction delays arise from either the atrioventricular node itself or along the His-Purkinje system. Unlike first-degree atrioventricular blocks and Mobitz I second-degree blocks, which occur in the atrioventricular node itself, Mobitz II blocks typically occur in an infranodal location, usually in the bundle branches or the Purkinje system. As a consequence, QRS widening or a bundle-branch pattern is often present. In 25% of patients, the block is in the His bundle, and the QRS complexes have normal morphology and duration (as was the case with this patient).[1,2,3]

Conduction delays can occur as a result of several medical conditions. Fibrosis, sclerodegenerative changes, and ischemic disease are the most common. Medication toxicities, including those associated with digitalis, verapamil, and beta-blockers, are also common causes. Other causes include cardiomyopathies, familial disease, increased vagal tone, hyperkalemia, and many other rare conditions. Coronary ischemia must be of highest concern because heart block secondary to infarction is associated with a high mortality rate.[1,2,3]

The treatment for atrioventricular block depends on the underlying etiology. It consists of correcting any reversible causes as well as providing supportive therapy, such as atropine, isoproterenol, and pacing. Atropine is often very helpful early on if the block is in the atrioventricular node or higher up the in the conduction system. Catecholamines (such as isoproterenol) can be transiently helpful no matter where the block appears to be; however, pharmacologic treatment with atropine or isoproterenol carries a potential for harm and should be used with caution. In general, these pharmacologic agents should be considered temporizing or bridging measures to a stabilizing temporary pacing system. Additionally, these agents are contraindicated in the setting of acute ischemic disease because they can increase myocardial oxygen demand. Unlike a Wenckebach pattern or a first-degree atrioventricular nodal block in which the direct effects of atropine at the node improve conduction, a Mobitz II block may not significantly respond to atropine because of its infranodal location. In fact, atropine may paradoxically exacerbate the block by allowing additional sinus impulses to pass the atrioventricular node, increasing the refractoriness of the infranodal tissues. If no improvement is seen after a cumulative dose of 2 mg of atropine, it should be discontinued. Isoproterenol may be used as a constant infusion starting at 0.5-2 ?g/min and titrated to 10 ?g/min to maintain a heart rate of 60 bpm.

Finally, transcutaneous or transvenous pacing is the definitive treatment and should be initiated in symptomatic patients, and even in asymptomatic patients, in anticipation of deterioration. A permanent pacemaker is placed after the patient's condition is sufficiently stabilized. A cardiologist should be consulted on an urgent basis for all patients with a Mobitz II block


 
 توقيع : د/منصور



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قديم 09-11-2012, 06:56 PM   #7


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

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افتراضي



( CASE NO .3 )

A 75-year-old man presents to the emergency department (ED) with a 6-week history of worsening lower abdominal pain. He describes the pain as sharp, constant, and associated with a weight loss of approximately 20 lb over the past month. The patient states that for the past few weeks he has also noticed bilateral lower-extremity swelling and abdominal distention. The abdominal distention has been severe enough to prevent him from bending over. He experienced an increased frequency of urination until 3 days ago; he has been anuric since then. For the past week he has not been able to tolerate solid foods, resulting in an entirely liquid diet. As of the day of presentation even liquids have become intolerable. There is also a history of numbness and tingling in both legs and an unsteady gait during the last week. He reports a feeling of confusion but is fully oriented to person, place, and time. His medical history is significant for hypertension under treatment and mitral valve insufficiency. He denies any surgical history. His current medications include daily aspirin and nifedipine. The patient has an age-appropriate level of physical activity and lives alone. He does not smoke or drink.
On physical examination, the patient is a well-oriented elderly man in no acute distress. His vital signs include an oral temperature of 97.4°F (36.3°C), a blood pressure of 211/92 mm Hg, a pulse of 104 beats/min, an unlabored respiratory rate of 20 breaths/min, and an oxygen saturation of 97% on room air. Head and neck examination reveals dry oral mucous membranes with a supple neck and no jugular venous distention. The chest examination is clear to auscultation bilaterally, with normal breath sounds and normal S1 and S2 heart sounds without murmurs, rubs, or gallops. The abdominal examination is significant for distention, mostly in the hypogastric and umbilical regions, and for the presence of a reducible umbilical hernia. Normal bowel sounds are appreciated in all quadrants. The patient's lower abdomen is diffusely tender, with slight tenderness noted in the upper abdomen as well. There is no rebound tenderness or guarding and Lloyd's sign is negative. Extremity examination is significant for bilateral pitting edema of the lower extremities. The patient has no focal neurologic abnormalities (although gait testing is deferred).
Initial laboratory investigations include a complete blood count (CBC) and basic metabolic panel. There are no significant findings on the CBC. The metabolic panel reveals a serum sodium level of 130 mEq/L (normal range, 136-145 mEq/L), potassium of 4.2 mEq/L (normal range, 3.5-5.0 mEq/L), chloride of 83 mEq/L (normal range, 95-105 mEq/L), bicarbonate of 16 mEq/L (normal range, 22-28 mEq/L), and glucose of 92 mg/dL (normal range, 70-125 mg/dL). Serum creatinine is 21.2 mg/dL (normal range, 0.6-1.2 mg/dL) and blood urea nitrogen is 120 mg/dL (normal range, 7-18 mg/dL). The calculated glomerular filtration rate (GFR) is 3 mL/min/1.73 m2 (normal, 90 mL/min/1.73 m2). A CT scan of the abdomen and pelvis is obtained


 
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قديم 09-11-2012, 07:07 PM   #8


الصورة الرمزية د/منصور
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The patient's CT scans both with and without contrast revealed moderate bilateral hydroureteronephrosis without evidence of an obstructing stone in the ureters. The kidneys were enlarged and perinephric fat stranding was noted (Figure 1). The prostate was also found to be enlarged and the bladder was noted to be extremely enlarged (Figure 2). A diagnosis of obstructive uropathy resulting from an enlarged prostate was made.
Total lower urinary tract obstruction (UTO) should be suspected when a patient presents with acute anuria and other causes, such as a past history of end stage renal disease (ESRD) or shock with prerenal failure, have been excluded. The most common cause of lower UTO in men is benign prostatic hyperplasia (BPH).[1] Other possible causes include phimosis, urethral strictures, and neurogenic bladder.


 
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قديم 09-11-2012, 07:10 PM   #9


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افتراضي



The clinical features of complete bilateral UTO include abdominal pain resulting from distention of the renal (Gerota) fascia or the urinary bladder, difficulty voiding, and hematuria.[4] Hypertension can result from increased renal secretion of renin.[3] Pain is less pronounced and may even go unnoticed in cases in which the obstruction progresses gradually. This can result in patients presenting after irreversible loss of renal function has already occurred. Frequent urinary tract infections or infections in uncommon populations, such as males and children, should raise suspicion for a partial or intermittent obstruction. Urine culture in these patients may reveal atypical organisms (such as Pseudomonas species


The diagnosis of UTO begins with the insertion of a bladder catheter; resulting diuresis suggests obstruction below the bladder. If catheterizing the bladder does not produce diuresis, a renal ultrasound can be used to confirm hydronephrosis with a sensitivity and specificity of 90%. False negatives on ultrasonography result from concomitant volume depletion, retroperitoneal fibrosis, obstructing malignancy, or if imaging is done too soon after the onset of an acute obstruction.[12] False positives occur in the setting of congenital anomalies and during diuresis.[13] In the setting of flank pain and suspicion for renal calculus without evidence of renal impairment, a kidneys-ureters-bladder x-ray will detect approximately 90% of renal stones.[3] Antegrade and retrograde urography can be used to determine the location of the urinary obstruction.).


 
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قديم 09-11-2012, 07:26 PM   #10


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



The management of UTO is directed by the underlying cause; however, regardless of the cause, relief of a prolonged period of obstruction with anuria is often accompanied by postobstructive diuresis. In most cases, this polyuria is transient and may be an adaptive response to fluid overload from the anuria, possibly compounded by iatrogenic fluid administration prior to the diagnosis of UTO. Routine monitoring of vital signs and serum electrolytes is important to assess possible volume depletion or the development of acquired DI.[14] The mechanism of this latter phenomenon is the same as that of the polyuria of partial UTO, manifesting as hypernatremia resistant to vasopressin. Alternatively, large sodium losses from tubular dysfunction will result in hyponatremia. If tachycardia and/or orthostatic hypotension develop following relief of the obstruction, pathologic hypovolemia secondary to diuresis and tubular damage should be suspected. In either of these instances, fluid and electrolyte correction are warranted; otherwise, fluid administration may only be serving to prolong the diuretic phase of the postobstructive recovery.[3,14]
The prognosis for the recovery of renal function is dependent upon the severity and duration of the obstruction. In addition, patients with obstruction complicated by pyelonephritis generally have a much worse outcome. Longstanding UTO leads to tubulointerstitial damage, which can ultimately result in ESRD. In the pediatric population, congenital urologic anomalies causing obstruction are the major cause of ESRD requiring dialysis.[15] With the exception of these risk factors, there is no way of accurately predicting to what degree renal function will be restored after an obstruction is removed


In the case presented, a Foley catheter was initially inserted, 2200 mL of urine were emptied, and the catheter was clamped. An hour later, 1700 mL were drained and the catheter was again clamped. A third drainage 50 minutes later yielded another 1000 mL. In total, 4900 mL of red-tinged urine was drained. The patient's abdominal distention promptly resolved with evacuation of the bladder, and the lower extremity edema regressed over the course of the patient's 4-day hospital stay. A review of the literature yielded case reports of similarly exaggerated urinary retention, including one case of a patient retaining more than 16 L over a 10-day period of anuria. The patient's creatinine levels dropped dramatically by the time of discharge and were within the normal reference range on follow-up 1 week after discharge.
.


 
 توقيع : د/منصور



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قديم 10-11-2012, 06:12 PM   #11


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



A 57-year-old man presents to the emergency department with left-sided facial, arm, and leg weakness along with slurred speech after suffering violent and repetitive bouts of coughing. His wife has the impression that his right eye is smaller than the left. The patient also complains of pain over his right eye. His medical history is notable for hypertension and smoking 1 pack of cigarettes per day for 10 years. He denies any illicit drug use. He does not consume alcohol. He is employed, does not exercise, and has a sedentary lifestyle. There is no history of previous head or neck injur

On physical examination, his oral temperature is 97.3°F (36.3°C). His pulse is regular with a rate of 94 bpm. His blood pressure is 195/105 mm Hg. The examination of his head and neck is normal. His lungs are clear to auscultation and have normal respiratory effort. No cardiac murmurs are detected. His abdomen is soft and nontender, with normal bowel sounds on auscultation. On neurologic examination, the patient is alert and oriented to time and place. His speech is slurred and dysarthric. On cranial nerve examination, the right pupil constricts from 2 mm to 1.5 mm in response to light, whereas the left pupil constricts from 3 mm to 2 mm. The right eyelid has 3 mm of ptosis compared with the left eye, and the right eye appears to be smaller than the left one. Pupillary asymmetry is more apparent when lights in the room are dimmed. Funduscopic examination reveals normal fundi. Visual acuity is normal bilaterally. The extraocular movements are intact. Facial sensation is decreased to light touch and pinprick on the left side. The patient has a decreased left nasolabial fold. He has weak movements of the left side of the face, without forehead involvement. The gag reflex is present, and there is normal palate elevation. After pinching the left side of the neck, the left pupil dilates normally (ciliospinal reflex). After pinching the right side of the neck, the right pupil does not dilate. He is unable to stand and walk. Muscular tone is flaccid on the left side but normal on the right. He has a marked left hemiparesis. The patient's reflexes are normal throughout except for an up-going plantar response on the left side, compared with a down-going one on the right. The patient reports decreased sensation to light touch, temperature, pinprick, joint position, and vibration on the left half of the body. His National Institute of Health Stroke Scale (NIHSS) is 11.


 
 توقيع : د/منصور



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قديم 10-11-2012, 06:16 PM   #12


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



Routine laboratory analyses are performed and result normal. Chest x-ray is normal. ECG shows left ventricular hypertrophy. A noncontrast CT scan of the head reveals a hyperdense right middle cerebral artery )

Conventional angiography reveals stenosis at the origin of right internal carotid artery, with an abrupt narrowing of its lumen ("rattail-filling defect";
)


 
 توقيع : د/منصور



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قديم 10-11-2012, 06:18 PM   #13


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



The patient in this case presented with a pattern of sensory loss and weakness on the left side of his body consistent with a lesion involving the right corticospinal and corticobulbar fibers and the primary somatosensory cortex. The most likely diagnosis was an ischemic stroke. Neurologic examination also revealed ptosis of the right eye with narrowing of the palpebral aperture, miosis in the right eye with a pupil that was reactive to light, and reduced ciliospinal reflex on pinching the right side of the neck. These signs are consistent with a partial Horner syndrome resulting from injury to sympathetic fibers traveling with the internal carotid artery. The sudden onset of neurologic deficits after violent coughing and the presence of pain over the patient's right eye are highly suggestive of a right internal carotid artery dissection. Conventional angiography was performed because the clinical findings were highly suspicious for an internal carotid artery dissection; this confirmed the diagnosis by showing an abrupt narrowing of the vessel's lumen ("rattail-filling defect"). The hyperdense middle cerebral artery revealed by noncontrast CT scan of the head suggested an occlusion of this artery. Laboratory analysis performed during hospitalization revealed the presence of mild hyperlipidemia. Screening analyses for hypercoagulability and rheumatologic disorders were normal. Transthoracic echocardiography was normal; however, duplex ultrasonographic imaging showed a stenosis in the right internal carotid artery.

Dissection of the internal carotid artery is an important cause of cerebrovascular disease in young adults. One study out of Rochester, Minnesota, showed an annual incidence of 2.6 patients out of 100,000 population. The actual incidence is difficult to evaluate, however, and may be higher because this condition, which may be asymptomatic or have various clinical presentations, may go unrecognized.[1] The incidence appears to have increased since the 1980s, but is likely due to the availability of better imaging studies.[1]

Dissection normally occurs in the extracranial segment of the epiaortic vessels. The internal carotid artery is affected more often than the vertebral artery.[2] Dissections can be classified as traumatic or spontaneous. Traumatic dissections are linked to direct neck trauma or injury, whereas spontaneous dissections may be secondary to predisposing factors, such as fibromuscular dysplasia, Ehlers-Danlos syndrome, cystic medial necrosis, or Marfan syndrome. These conditions cause an abnormal, weakened arterial wall, thus predisposing patients to arterial dissection.[3]

Internal carotid artery dissection develops as a consequence of a tear in the intimal layer of the vessel, which allows blood to enter the wall of the artery and to split its layers, which is termed a subintimal hematoma. This means that the hematoma is located between the intimal and medial layers of the artery. Alternatively, a rupture of the vasa vasorum causes a subadventitial hematoma (ie, a hematoma between the media and the adventitial layers). Internal carotid artery dissection can lead to thrombus formation and the risk for distal embolization, whereas arterial narrowing with stroke due to inadequate blood flow is a less common mechanism of ischemia.[4] Hematoma formation and a localized inflammatory response result in compression of nearby structures, such as the sympathetic fibers of the superior cervical ganglion, which lies in the posterior wall of the carotid sheath. This can cause a postganglionic oculosympathetic palsy. There is no anhidrosis because sweat fibers run with the uninvolved external carotid artery.

The most typical signs and symptoms of internal carotid artery dissection are neck pain and/or a partial Horner syndrome. This may be followed by an ischemic event ipsilateral to the ocular signs, with somatosensory and/or motor deficits contralateral to ocular signs as a consequence of distal embolization to the intracerebral arteries.

A highly suggestive constellation of signs and symptoms frequently seen with internal carotid artery dissection is Horner syndrome. Oculosympathetic palsy in the form of Horner syndrome has long been recognized as a typical manifestation of internal carotid artery dissection, although it is found in fewer than half of patients. The classic signs of Horner syndrome are ptosis of the upper lid, slight elevation of the lower lid (upside-down ptosis), and miosis reactive to light. The narrow palpebral aperture secondary to upper-lid ptosis and elevation of the lower lid give the illusion that the affected eye is smaller than the contralateral eye (illusory enophthalmos). Horner syndrome is an expression of a disruption of oculosympathetic pathways. Ptosis (ie, upper eyelid droop) is caused by a loss of innervation to Müller's smooth muscle in the upper lid. This small muscle is innervated by sympathetic fibers and is responsible for eye opening, together with the superior and levator palpebrae: striated skeletal muscle innervated by the third cranial nerve. Similarly, miosis (ie, decreased papillary size) is caused by a loss of sympathetic innervation to the iris pupillodilator muscle. As a consequence, the pupil cannot dilate. This impaired dilation of the pupil may also be observed in a test of the ciliospinal reflex. Normally, pinching the neck causes a papillary dilation secondary to the activation of sympathetic pathway. In an eye with Horner syndrome, this dilation does not occur.

Currently, the most commonly available imaging modalities are carotid ultrasonography and CT angiography (CTA) of the head and neck. However, the best method to diagnose an internal carotid artery dissection is a combination of CTA and magnetic resonance angiography (MRA) with fat-suppressed T1 CTA and MRA are replacing conventional angiography in the diagnosis of internal carotid and vertebral artery dissection because the resolution and accuracy of CTA and MRA are similar to that of angiography.[7-9] Moreover, MRI may show the intramural hematoma itself. As an alternative, conventional angiography with digital subtraction may be used, although these tests are more expensive and invasive than MRI/MRA. Additionally, MRI/MRA is superior to conventional angiography in diagnosing dissections without associated luminal abnormalities.[1] Conventional angiography may reveal an abrupt narrowing of the internal carotid artery lumen (rattail-filling defect or the "string sign"). Carotid duplex ultrasonographic imaging may also be useful, especially in the younger population, with less chance of severe atherosclerotic disease, which can interfere in the diagnosis.[10] Direct observation of a luminal intimal flap is diagnostic but rare; the most frequent finding is a stenosed or occluded vessel in the absence of atheromatous lesions.]


 
 توقيع : د/منصور



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قديم 10-11-2012, 06:23 PM   #14


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



The treatment of internal carotid artery dissection consists of anticoagulation with intravenfollowed by oral anticoagulation for 3-6 months.[13] However, there are no randomized controlled trials supporting such a therapeutic approach, and the validity of such treatment has never been definitively proven.

The patient in this case was first treated withous heparin intravenous heparin followed by oral anticoagulation in order to prevent distal embolization. He continued anticoagulant therapy for 3 months. The patient's Horner syndrome resolved completely after 3 days, but the left-sided sensorimotor deficits persisted at discharge


 
 توقيع : د/منصور



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قديم 11-20-2012, 09:11 AM   #15


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي




acute diarrhoeal disease

In 2003 the Center for Disease Control (CDC) put forth recommendations for the management of acute pediatric diarrhea in both the outpatient and inpatient settings including indication for referral.[7]
Indications for medical evaluation of children with acute diarrhea include the following
:
  • Younger than 3 months
  • Weight of less than 8 kg
  • History of premature birth, chronic medical conditions, or concurrent illness
  • Fever of 38***186;C or higher in infants younger than 3 months or 39***186;C or higher in children aged 3-36 months
  • Visible blood in the stool
  • High-output diarrhea
  • Persistent emesis
  • Signs of dehydration as reported by caregiver, including sunken eyes, decreased tears, dry mucous membranes, and decreased urine output
  • Mental status changes
  • Inadequate responses to oral rehydration therapy (ORT) or caregiver unable to administer ORT

The report also includes information on assessment of dehydration and what steps should be taken to adequately treat acute diarrhea.
Treatment of dehydration due to diarrhea includes the following:
  • Minimal or no dehydration
    • Rehydration therapy - Not applicable
    • Replacement of losses
      • Less than 10 kg body weight - 60-120 mL oral rehydration solution for each diarrhea stool or vomiting episode
      • More than 10 kg body weight - 120-140 mL oral rehydration solution for each diarrhea stool or vomiting episode
  • Mild-to-moderate dehydration
    • Rehydration therapy - Oral rehydration solution (50-100 mL/kg over 3-4 h)
    • Replacement of losses
      • Less than 10 kg body weight - 60-120 mL oral rehydration solution for each diarrhea stool or vomiting episode
      • More than 10 kg body weight - 120-140 mL oral rehydration solution for each diarrhea stool or vomiting episode
  • Severe dehydration
    • Rehydration therapy - Intravenous lactated Ringer solution or normal saline (20 mL/kg until perfusion and mental status improve), followed by 100 mL/kg oral rehydration solution over 4 hours or 5% dextrose (half normal saline) intravenously at twice maintenance fluid rates
    • Replacement of losses
      • Less than 10 kg body weight - 60-120 mL oral rehydration solution for each diarrhea stool or vomiting episode
      • More than 10 kg body weight - 120-140 mL oral rehydration solution for each diarrhea stool or vomiting episode
      • If unable to drink, administer through nasogastric tube or intravenously administer 5% dextrose (one fourth normal saline) with 20 mEq/L potassium chloride

ORT is the cornerstone of treatment, especially for small-bowel infections that produce a large volume of watery stool output. ORT with a glucose-based oral rehydration syndrome must be viewed as by far the safest, most physiologic, and most effec*tive way to provide rehydration and maintain hydration in children with acute diarrhea worldwide, as recommended by the WHO; by the ad hoc committee of European Society for Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN); and by the American Academy of Pediatrics.[8] However, the global use of ORT is still insufficient. Developed countries, in particular the United States, seem to be lagging behind despite studies that demonstrate beyond doubt the efficacy of ORT in emergency care settings, in which intravenous rehydration unduly continues to be widely privileged.
Not all commercial ORT formulas promote optimal absorption of electrolytes, water, and nutrients. The ideal solution has a low osmolarity (210-250) and a sodium content of 50-60 mmol/L. Administer maintenance fluids plus replacement of losses. Educate caregivers in methods necessary to replace this amount of fluid. Administer small amounts of fluid at frequent intervals to minimize discomfort and vomiting. A 5-mL or 10-mL syringe without a needle is a very useful tool. The syringe can be quickly used to place small amounts of fluid in the mouth of a child who is uncooperative. Once the child becomes better hydrated, cooperation improves enough to take small sips from a cup. This method is time intensive and requires a dedicated caregiver. Encouragement from the physician is necessary to promote compliance. Oral rehydration is now universally recommended to be completed within 4 hours.
The addition of zinc to oral rehydration solution has been proven effective in children with acute diarrhea in developing countries and is recommended by the WHO.[9] However, no evidence suggests efficacy in children living in developed countries, in which the prevalence of zinc deficiency is assumed to be extremely low.
The composition of almost all other beverages (carbonated or not) that are commercially available and frequently used in children with diarrhea is completely inadequate for rehydration or for maintaining hydration, considering the sodium content, which is invariably extremely low, and osmolarity that is often dangerously elevated. For instance, Coca-Cola, Pepsi-Cola, and apple juice have an osmolarity of 493, 576, and 694-773, respectively.
At completion of hydration, resumption of feeding is strongly recommended. In fact, many studies convincingly demonstrate that early refeeding hastens recovery. Also, robust evidence suggests that, in the vast majority of episodes of acute diarrhea, refeeding can be accomplished without the use of any special (eg, lactose-free or soy-based) formulas
.


نقرتين لعرض الصورة في صفحة مستقلة

نقرتين لعرض الصورة في صفحة مستقلة


 
 توقيع : د/منصور



رد مع اقتباس
قديم 11-20-2012, 09:20 AM   #16


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



Antimotility agents are not indicated for infectious diarrhea, except for refractory cases of Cryptosporidium infection. Antimicrobial therapy is indicated for some nonviral diarrhea because most is self-limiting and does not require therapy.
Therapies recommended for some nonviral diarrheas include the following:
  • Aeromonas species: Use cefixime and most third-generation and fourth-generation cephalosporins.
  • Campylobacter species: Erythromycin shortens illness duration and shedding.
  • C difficile: Discontinue potential causative antibiotics. If antibiotics cannot be stopped or this does not result in resolution, use oral metronidazole or vancomycin. Vancomycin is reserved for the child who is seriously ill.
  • C perfringens: Do not treat with antibiotics.
  • Cryptosporidium parvum: Administer paromomycin; however, effectiveness is not proven. Nitazoxanide, a newer anthelmintic, is effwed by iodoquinol or paromomycin is administered in symptomatic patients. Asymptomatic carriers in nonendemic areas should receive iodoquinol or paromomycin.
E coli: Trimethoprim-sulfamethoxazole (TMP-SMX) should be administered if moderate or severe diarrhea is noted; antibiotic treatment may increase likelihood of hemolytic-uremic syndrome (HUS). Parenteral second-generation or third-generation cephalosporin is indicated for systemic complications.
  • G lamblia: Metronidazole or nitazoxanide can be used.
  • Plesiomonas species: Use TMP-SMX or any cephalosporin.
  • Salmonella species: Treatment prolongs carrier state, is associated with relapse, and is not indicated for nontyphoid-uncomplicated diarrhea. Treat infants younger than 3 months and high-risk patients (eg, immunocompromised, sickle cell disease). TMP-SMX is first-line medication; however, resistance occurs. Use ceftriaxone and cefotaxime for invasive disease.
  • Shigella species: Treatment shortens illness duration and shedding but does not prevent complications. TMP-SMX is first-line medication; however, resistance occurs. Cefixime, ceftriaxone, and cefotaxime are recommended for invasive disease.
  • V cholerae: Treat infected individuals and contacts. Doxycycline is the first-line antibiotic, and erythromycin is second-line antibiotic.
  • Yersinia species: TMP-SMX, cefixime, ceftriaxone, and cefotaxime are used. Treatment does not shorten disease duration; reserve for complicated cases.



نقرتين لعرض الصورة في صفحة مستقلة


 
 توقيع : د/منصور



رد مع اقتباس
قديم 11-20-2012, 09:25 AM   #17


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



Diet

Breastfed infants with acute diarrhea should be continued on breast milk without any need for interruption. In fact, breastfeeding not only has a well-known protective effect against the development of enteritis, it also promotes faster recovery and provides improved nutrition. This is even more important in developing countries, where with*drawal of breastfeeding during diarrhea has been shown to have a deleterious effect on the development of dehydra*tion in infants with acute watery diarrhea.
  • Bananas, rice, applesauce, and toast diet
    • A banana, rice, applesauce, and toast (BRAT) diet was introduced in the United States in 1926 and has enjoyed vast popularity. However, no evidence shows that this diet is useful, and its poor protein content may be a contraindication; therefore, it is not recommended.
    • A strong body of evidence now suggests that resuming the prediarrhea diet is perfectly safe and must be encouraged, obviously respecting any (usually temporary) lack of appetite.
  • Lactose ingestion
    • Although rotavirus can cause secondary transient lactose intolerance, this finding is believed to be generally not clinically relevant; use lactose-containing formulas in all individuals with diarrhea.
    • In an incident of worsening of diarrhea proven to be secondary to a clinically important lactose malabsorption in infants positive for rotavirus, a very transient use of lactose-free formulas (5-6 d) can be considered.


نقرتين لعرض الصورة في صفحة مستقلة نقرتين لعرض الصورة في صفحة مستقلة
نقرتين لعرض الصورة في صفحة مستقلة


 
 توقيع : د/منصور



رد مع اقتباس
قديم 11-20-2012, 09:28 AM   #18


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



Medication Summary

Diarrheal diseases have been the object of numerous forms of treatment, both dietetic and pharmacologic, for centuries. However, the evidence is now clear that, in most cases, the best option for treatment of acute-onset diarrhea is the early use of oral rehydration therapy (ORT).[7] Pharmacological treatment is rarely of any use, and antidiarrheal drugs are often harmful
In terms of recommended antimicrobial treatment in the immunocompetent host, enteric bacterial and protozoan pathogens can be grouped as follows
Agents for whom antimicrobial therapy is always indicated: The consensus includes only V cholerae, Shigella species, and G lamblia.
Agents for whom antimi*crobial therapy is indicated only in selected circumstances, include the following
  • Infections by enteropathogenic E coli, when running a prolonged course
  • Enteroinvasive E coli, based on the sero*logic, genetic, and pathogenic similarities with Shigella
  • Yersinia infections in subjects with sickle cell disease
  • Salmonella infections in very young infants, if febrile or with positive blood culture findings


 
 توقيع : د/منصور



رد مع اقتباس
قديم 11-20-2012, 09:32 AM   #19


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



Consider consultation with an infectious-disease specialist for any patient who is immunocompromised because of HIV infection, chemotherapy, or immunosuppressive drugs because atypical organisms are more likely, and complications can be more serious and fulminate


 
 توقيع : د/منصور



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قديم 02-04-2013, 05:55 PM   #20


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
افتراضي



Q. My 2-year-old daughter had a seizure and a fever and she was sent to the ER. They sent us home, but now I'm wondering if she's going to have another one or how should she feel now because she is so fussy. She only wants to be carried by me and cries all day long. What do I do? Elizabeth, San Bernardino, CA


febrile seizures (a seizure that is caused by a fever) are usually not serious.

They usually occur in young children, during a viral illness in which their fever spikes up high all of a sudden. About 2% to 5% of children have febrile seizures.

Children who have febrile seizures have a very small risk of later developing regular seizures, but according to the National Institute of Neurological Disorders and Stroke, 'between 95% to 98% of children who have experienced febrile seizures do not go on to develop epilepsy.'

These children are at risk for having more febrile seizures though. In fact, about one=third of children who have febrile seizures go on to have another one later on. Fortunately, most children outgrow having febrile seizures by the time they are about 5 years old.

Remember that febrile seizures are not harmful though and they do not cause brain damage
>.


 
 توقيع : د/منصور



رد مع اقتباس
قديم 02-04-2013, 05:57 PM   #21


الصورة الرمزية د/منصور
د/منصور غير متواجد حالياً

بيانات اضافيه [ + ]
 رقم العضوية : 7684
 تاريخ التسجيل :  Dec 2010
 أخر زيارة : 06-06-2022 (11:39 AM)
 المشاركات : 1,862 [ + ]
 التقييم :  50
 الدولهـ
Saudi Arabia
 الجنس ~
Male
لوني المفضل : Blueviolet
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First Aid for Febrile Seizures

If your child is having a febrile seizure, according to the National Institute of Neurological Disorders and Stroke, you should "stay calm and carefully observe the child. To prevent accidental injury, the child should be placed on a protected surface such as the floor or ground. The child should not be held or restrained during a convulsion. To prevent choking, the child should be placed on his or her side or stomach. When possible, the parent should gently remove all objects in the child's mouth. The parent should never place anything in the child's mouth during a convulsion. Objects placed in the mouth can be broken and obstruct the child's airway. If the seizure lasts longer than 10 minutes, the child should be taken immediately to the nearest medical facility for further treatment. Once the seizure has ended, the child should be taken to his doctor to check for the source of the fever. This is especially urgent if the child shows symptoms of stiff neck, extreme lethargy, or abundant vomiting."


 
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قديم 02-04-2013, 06:02 PM   #22


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Medical Treatment for Febrile Seizures


Although febrile seizures are not harmful and usually don't require any treatment, the concern comes when your Pediatrician is not sure that your child is in fact having a simple febrile seizures. Although a child has both a fever and a seizure, it is sometimes possible that a child has something else, like meningitis, causing both and that the fever didn't trigger the seizure. In this case, further testing, like a spinal tap, might be done, especially in children younger than 12 to 18 months old. Blood and urine tests may also be done in some situations.
Most children with simple febrile seizures, who aren't too fussy and appear well after the seizure, don't require any testing though. In fact, that American Academy of Pediatrics recommends that other tests, like an EEG, CT, or MRI, not routinely be done in children with a first simple seizur
e.


 
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قديم 02-04-2013, 06:08 PM   #23


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Preventing Febrile Seizures


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The only real way to prevent febrile seizures is to try and avoid allowing your child to get sick, which might lead to a fever, in the first place. Giving a fever reducer, such as Tylenol (acetaminophen) or Motrin (ibuprofen), at the first sign of a fever is often recommended, but likely won't prevent a febrile seizure.
Some children who have a lot of febrile seizures are treated with Diazepam at the first sign that they have a fever, but this usually isn't necessary. Apediatric neurologist can be helpful if you think your child needs treatment for her febrile seizures
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قديم 02-19-2013, 02:30 PM   #24


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CHANCE: Clopidogrel plus aspirin lowered risk for second stroke




  • February 11, 2013
Adding clopidogrel to aspirin therapy in the weeks following a minor stroke or transient ischemic attack reduced the risk for a second stroke by more than 30%, according to results from the CHANCE trial presented at the International Stroke Conference 2013.

Researchers studied 5,170 Chinese patients (mean age, 62 years; 34% women) who had a minor ischemic stroke or TIA. Patients were randomly assigned within 24 hours of symptom onset to a Clopidogrel300-mg loading dose followed by 75 mg daily plus aspirin 75 mg for the first 21 days or to aspirin alone. On day 1, all patients received open-label aspirin 75 mg to 300 mg. The primary outcome was stroke (ischemic or hemorrhagic) during 90 days of follow-up.
Stroke occurred in 11.7% of the aspirin alone group compared with 8.2% of the clopidogrel plus aspirin group (HR=0.68; 95% CI, 0.57-0.81). Both groups experienced similar occurrence of moderate or severe stroke (0.3%) and hemorrhagic stroke (0.3%).
“[These data] suggest that combination therapy is more effective than aspirin alone, and is a safe treatment,” S. Claiborne Johnston, MD, PhD, professor of neurology and director of the stroke service at University of California, San Francisco, said at a press conference.
According to Yongjun Wang, MD, professor of neurology and vice president of Beijing TianTan Hospital, Capital Medical University, China, “In China, stroke and mini-stroke patients are 6 to 8 years younger, on average, than Americans, and there are different genetic variations that have an impact on the metabolism of clopidogrel.”
Johnston said he suspects that these data will also apply to patients and clinical settings in the United States, and data from the ongoing POINT trial will provide more information on dual therapy in this patient populatio


 
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قديم 04-01-2013, 06:41 PM   #25


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Lisfranc Fracture Dislocations






 
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قديم 04-01-2013, 07:30 PM   #26


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Lisfranc Fracture Dislocations

http://www.viewdocsonline.com/document/xd17mq


 
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قديم 04-01-2013, 08:17 PM   #27


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نقرتين لعرض الصورة في صفحة مستقلة

نقرتين لعرض الصورة في صفحة مستقلة

نقرتين لعرض الصورة في صفحة مستقلة

نقرتين لعرض الصورة في صفحة مستقلة


 
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قديم 05-08-2013, 03:34 PM   #28


tasneem غير متواجد حالياً

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بعد التحية و السلام عليكم,,
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قديم 05-09-2013, 08:45 PM   #29


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[QUOTE=تسنيم عثمان;241482]بعد التحية و السلام عليكم,,
شكرا: جزيلا" دكتور منصور استفدنا جدا" من هذا الموضوع خاصة و انا اسعى لعمل اكبر collections of case discussion ربنا يجعله في ميزان حسناتك.

مرحب بيك تسنيم عثمان ..مشكورة على المرور ..ربنا يوفقك واى مساعدة نحن جاهزين.تحياتى لك.


 
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قديم 10-25-2013, 11:28 PM   #30


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Sudden infant death syndrome (SIDS), also known as cot death, is the sudden, unexpected and unexplained death of an apparently well baby.
In the UK, at least 300 babies die suddenly and unexpectedly every year. Despite these deaths, SIDS is rare and the risk of your baby dying from it is low.
Most deaths happen during the first three months of a baby’s life. Infants born prematurely or with a low birth weight are at greater risk, and SIDS is also more common in baby boys.
Most unexpected deaths occur while the child is asleep in their cot at night. However, SIDS can also occur when a baby is asleep during the day or, occasionally, while they are awake.
Mothers can reduce the risk of SIDS by not smoking while pregnant or after the baby is born, and always placing the baby on their back when they sleep).
?What causes SIDS

No one knows exactly what causes SIDS, but it is thought to be the result of a combination of factors.
Experts believe SIDS occurs at a particular stage in a baby’s development, and that it affects babies who are vulnerable to certain environmental stresses.
This vulnerability may be due to being born prematurely or to low birth weight, or other reasons not yet identified.
Environmental stresses could include tobacco smoke, getting tangled in bedding, minor illness or having a breathing obstruction
Babies who die of SIDS are thought to have problems in the way they respond to these stresses and how they regulate their heart rate, breathing and temperature.
Although the cause of SIDS is not fully understood, you can reduce the risk).
?What can I do to help prevent SIDS

Follow the advice below to help prevent SIDS.
Place your child on their back to sleep. The safest place for them to sleep is in a cot in a room with you for the first six months
Do not smoke while you are pregnant or after your baby is born, and do not let anyone else smoke in the same room as your baby
Do not share a bed with your baby, particularly if you have been drinking alcohol or taking drugs
Never sleep with your baby on a sofa or an armchair.
Do not let your baby get too hot.
Keep your baby’s head uncovered. Their blanket should be tucked in no higher than their shoulders
If possible, breastfeed your baby.
d


 
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