Source:http://drcd2009.wordpress.com/
C – caustic/corrosive agents
H – heavy metals
A – alcohols and glycols/absent bowel sounds
R – rapidly absorbed substances
C – cyanide
O – other insoluble drugs/obstructed bowel
A – aliphatic hydrocarbons
L – laxatives
 |  |  | |
| Percentage | 60 % | 10-15 % | 25-30 % |
| Type | DeBakey I | DeBakey II | DeBakey III |
| Stanford A | Stanford B | ||
| Proximal | Distal | ||
| Classification of aortic dissection | |||
The criteria demonstrated 96% sensitivity (95% confidence interval [CI], 92% to 100%) and 62% specificity (95% CI, 58% to 66%) for serious outcomes at 7 days
Stickberger SA, Benson W, Biaggioni I, et al. AHA/ACCF scientific statement on the evaluation of syncope. J Am Coll Cardiol. 2006;12:473-484
Caution:
Up to 11% of patients discharged home with 0 out of 5 on the “CHESS” algorithm may still have a serious outcome as defined in the study within 30 days — an unacceptably high risk
Miller CD, Hoekstra JW. Prospective validation of the San Francisco Syncope Rule: Will it change practice [Editorial]? Ann Emerg Med. 2006;47:455-456
A 2007 consensus document classifies myocardial infarction into five main types:
* Type 1 - Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
* Type 2 - Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
* Type 3 - Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
* Type 4 - Associated with coronary angioplasty or stents:
o Type 4a - Myocardial infarction associated with PCI
o Type 4b - Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy
* Type 5 - Myocardial infarction associated with CABG
Source:http://emedicine.medscape.com/article/92337-overview
Introduction
Injuries in and around the shoulder are common in today's athletic society. Proper knowledge of the different problems and treatment options for shoulder disorders is necessary to get patients back to their preinjury state.
Background
Acromioclavicular (AC) joint injuries are common and often seen after bicycle wrecks, contact sports, and car accidents. The acromioclavicular joint is located at the top of the shoulder where the acromion process and the clavicle meet to form a joint. Several ligaments surround this joint, and depending on the severity of the injury, a person may tear one or all of the ligaments. Torn ligaments lead to acromioclavicular joint sprains and separations.1
Contents |
Kernohan's notch phenomenon is a result of the compression of the cerebral peduncle, which is part of the mesencephalon, against the tentorium due to transtentorial herniation. This produces ipsilateral hemiparesis or hemiplegia[5]
The skull is an in compressible closed space with a limited volume (Monro-Kellie Doctrine). When there is increased cranial pressure in the brain, a shift in the brain forms towards the only opening of the skull, the foramen magnum. Thus, when an increase of pressure in a hemisphere of the brain exists, the cerebral peduncle on the opposite hemisphere is pushed up against the tentorium, which separates the posterior fossa from the anterior fossa. This produces a visible "notch" in the cerebral peduncle.[6] Because of the fact that a Kernohan's notch is caused by an injury creating pressure on the opposite hemisphere of the brain, it is characterized as a false localizing sign.[7]
The Kernohan's notch phenomenon is unique in that it is not only a false localizing sign, but is also ipsilateral or same-sided. The left cerebral peduncle contains motor fibers that cross over to the right side of the body. Thus, if you have a right hemisphere problem, it causes a Kernohan's notch in the left cerebral peduncle which results in right-sided motor impairment. Therefore you get, paradoxically, impairment of motor function on the same side of the body as the injury causing the Kernohan's notch.[8]
The Kernohan's notch is a secondary phenomenon that results from a major primary injury. Non-tumoral, non-traumatic, intracranial haemorrhage rarely causes this phenomenon.
A wide range of serious injuries can cause an increase in intracranial pressure to trigger the formation of a Kernohan's notch. In general, this phenomenon occurs in patients with advanced brain tumor or severe head injury.[9] In the case of severe head injury, a clot can occur over the surface of the brain and can often cause shift of the middle part of the brain against the tentorium, which creates the Kernohan's notch. Chronic subdural hematomas have been known to be a familiar cause of Kernohan's notch.[10]
MRIs have shown evidence of Kernohan's notch from patients with traumatic head injury that are related to acute space-occupying lesions such as subdural hematoma, epidural hematoma, depressed skull fracture, or spontaneous intracerebral hematoma.[11][12]
Also, it is important to note that the anatomical size of tentorial notches vary considerably between individuals; however, very little evidence supports that a more narrow notch creates a predisposition towards Kernohan's notch.[13]
Symptoms directly related to the Kernohan's notch is most commonly paralysis or weakness on one side of the body.[14] Paralysis and weakness is known as hemiplegia and hemiparesis, respectively. This is due to destruction or pressure applied to the motor fibers located in the cerebral peduncle. A more rare sign of Kernohan's notch is ipsilateral oculomotor nerve palsy.[15]
However, most patients come into the clinic citing symptoms associated with the primary injury causing the Kernohan's notch. Since so many types of head injuries exist, virtually any symptom of brain trauma can be seen accompanying Kernohan's notch. These symptoms may range from total paralysis to simple headache, nausea, and vomiting.[16]
Because of the ipsilateral characteristic of Kernohan's notch, diagnosis is unique. Many clinicians assume a right sided paralysis corresponds with an injury in the left hemisphere of the brain and misdiagnose Kernohan's notch.[17] Despite this complication that ipsilateral paralysis causes, it makes it very easy to diagnose when coupled with imaging techniques. For example, when seeing an MRI of a blood clot on the left side of the brain coupled with left-sided paralysis, it immediately points to Kernohan's notch.
In most head trauma cases, CT scans are the standard diagnostic method; however it is not ideal for imaging small lesions, so MRI is used to identify Kernohan's notch. It is important to distinguish Kernohan's notch from direct brain stem injuries. Case studies have shown that in patients with chronic subdural hematoma, a compressive deformity of the crus cerebri without an abnormal MRI signal may predict a better recovery in patients with Kernohan's notch.[18]
There is no special treatment for Kernohan's notch since treatment is completely dependent on the injury causing it. The pressure against the tentorium should be relieved and the notch should go away. However, this does not mean that damage to the motor fibers disappears. Depending on the severity of the injury, there may or may not be persistent damage after pressure relief. Neurological deficits may resolve after surgery, but some degree of deficit, especially motor weakness, generally remains.[19]
Pressure relief to "un-notch" the cerebral peduncle may include the removal of brain tumors and blood clots or the suction of blood from a drilled hole in the skull.[20]
The ipsilateral and false localizing signs characteristic of Kernohan's notch sometimes cause confusion and result in misdiagnosis. Such a case is described in an account by Wolf at the University Hospital in Groningen, Netherlands[21]:
Kernohan's notch phenomenon associated with a ruptured arteriovenous malformation (AVM) is rare, but not unknown. This was accounted for in a case study described by Fujimoto at the Tsukuba Memorial Hospital in Ibaraki, Japan[22]:
One of the first references to casual brain herniation was that of James Colier, who clearly described cerebellar tonsilar herniation in 1904.[23] He observed accompanying false localyzing signs and commented:
In 1920, Adolf Meyer confirmed the pathologies of brain herniation.[24] He commented:
The work of Collier and Meyer described ipsilateral hemiparesis, a false localizing sign. However, it became known as the Kernohan-Woltman phenomenon.[25]
In 1929, Kernohan and Woltman published their work on brain lesions that showed ipsilateral hemiplegia.[26] In their paper, they state:
Kernohan fully described the Kernohan's notch in 1929 and is given credit for its discovery.
| Brain: Tentorium cerebelli | ||
|---|---|---|
 | ||
 | ||
| Tentorium cerebelli seen from above. | ||
| subject #193 874 | ||
| Meninges | ||
| ancil-261 | ||
The tentorium cerebelli or cerebellar tentorium (Latin: "tent of the cerebellum") is an extension of the dura mater that separates the cerebellum from the inferior portion of the occipital lobes.
The tentorium cerebelli is an arched lamina, elevated in the middle, and inclining downward toward the circumference.
It covers the superior surface of the cerebellum, and supports the occipital lobes of the brain.
Its anterior border is free and concave, and bounds a large oval opening, the incisura tentorii, for the transmission of the cerebral peduncles.
It is attached, behind, by its convex border, to the transverse ridges upon the inner surface of the occipital bone, and there encloses the transverse sinuses; in front, to the superior angle of the petrous part of the temporal bone on either side, enclosing the superior petrosal sinuses.
At the apex of the petrous part of the temporal bone the free and attached borders meet, and, crossing one another, are continued forward to be fixed to the anterior and posterior clinoid processes respectively.
To the middle line of its upper surface the posterior border of the falx cerebri is attached, the straight sinus being placed at their line of junction.
Clinically, the tentorium is important because brain tumors are often characterized as supratentorial (above the tentorium) and infratentorial (below the tentorium). The location of the tumor can help in determining the type of tumor, as different tumors occur with different frequencies at each location. Additionally, most childhood tumors are infratentorial, while most adult tumors are supratentorial. The location of the tumor may have prognostic significance as well.
Since the tentorium is a hard structure, if there is a volume expansion in the parenchyme above the tentorium, the brain can get pushed down partly through the tentorium. This is called herniation and will often give mydriasis on the affected side, due to pressure on cranial nerve III (N. Oculomotorius). Tentorial herniation is a serious symptom, especially since the brainstem is likely to be compressed as well if the intracranial pressure rises further.
Source:http://www.emedmag.com/html/pre/fea/features/038120044.asp
When Is Venous Blood Gas Analysis Enough?
Since venipuncture is less painful, less costly, and safer for the practitioner, do you really need that arterial blood sample? The authors explain why, in many cases, the answer is no.
By Scott C. Sherman, MD, and Michael Schindlbeck, MD
A 34-year-old man with a history significant for diabetes mellitus presents to the emergency department after experiencing progressive abdominal pain and vomiting for three days. His medications include insulin, but he states that he has missed several doses. A bedside glucose level taken in triage is 532 mg/dl. The patient appears to be in moderate discomfort with dry mucous membranes. His blood pressure is 118/80 mmHg; his heart rate, 124. He is in no apparent respiratory distress, but his respiratory rate is 22. Pulse oximetry reading on room air is 97%.
You order routine lab tests and a fluid bolus, then search for an arterial blood gas (ABG) kit. Just as you are about to draw blood from the patient’s radial artery, the nurse asks if you would like to order a venous blood gas (VBG) along with the cell count and chemistries.
CORNERSTONE OF MANAGEMENT
Recent studies have questioned this dogma, however. In specific scenarios, a VBG analysis may provide enough information to make the correct diagnosis and begin appropriate therapy.
In this article, we will review the practical advantages of VBG analysis and discuss its utility in the management of both metabolic and respiratory acid-base disorders.
advantages of vbg analysis
Blood gas analysis provides a great deal of data in a short period of time. When it has been set up in the emergency department as a point-of-care test, results can be obtained in about two minutes. In addition, most analyzers give more information than just the patient’s pH, PO2, PCO2, and HCO3. Other data include hemoglobin, sodium, potassium, glucose, methemoglobin, carboxyhemoglobin, ionized calcium, and lactate levels.
The most obvious advantage to obtaining a VBG instead of an ABG is decreased pain for the patient. A 1996 double-blinded study by Giner found that pain scale ratings were reduced by almost half with VBG compared to ABG. (There was no significant difference in the ratings when a local anesthetic had been used prior to an arterial blood draw, but this is not always done.)
Also, a VBG sample can be drawn using the same intravenous (IV) line that is used to draw blood for other lab tests, thus necessitating only one puncture. This translates into decreased costs, labor, and risk of needlestick injury to the health care provider. Furthermore, complications such as arterial laceration, hematoma, and thrombosis are all but negated with venous blood sampling.
CRITICAL ILLNESS AND CARDIAC ARREST
So VBG analysis has several obvious advantages over ABG. But what about the data obtained with ABG analysis? Is it unique? Is it diagnostically superior to the data obtained with venous blood sampling?
Normal values for pH, PO2, PCO2, and HCO3 in healthy individuals are listed in the table (below). However, because emergency department patients are generally not healthy, it is important to compare arterial and venous values in acutely ill individuals. A 1985 study by Gennis of critically ill emergency department patients revealed a breakdown in the linear relationship between arterial and venous values for pH, PCO2, and HCO3 seen in healthy individuals. However, the study did demonstrate that normal venous pH, PCO2, and HCO3 ruled out severe acid-base disturbances. For example, a venous pH of 7.25 or higher predicted an arterial pH of 7.2 or higher in 98% of all cases, which makes VBG testing valuable as a screening procedure. If the results are normal, ABG analysis should not be necessary. Conversely, abnormal venous levels predicted abnormal arterial values, but again in a nonlinear fashion. A venous pH of 7 or lower, for example, predicted an arterial pH of 7.2 or lower in 98% of cases.
In cardiac arrest victims, the disparity between arterial and venous values is even greater. During cardiac arrest, tissue hypoxia is all but a certainty and is reflected by the lower pH and higher PCO2 on the venous side. A 1986 study by Weil demonstrated a significantly lower pH in venous samples (mean, 7.15 vs 7.41 in arterial samples) and a significantly elevated PCO2 (mean, 74 mm Hg vs 32 mm Hg) in these patients. In clinical practice, however, knowledge of either the arterial or venous pH or PCO2 during cardiac arrest does not alter management, making the debate less relevant.
A similar 1989 study by Androque confirmed the above findings in cardiac arrest, but it also included patients in severe hemodynamic failure not related to cardiac arrest. The study found that as cardiac output declines, the differences between arterial and venous measurements increase. These authors concluded that VBG analysis in cardiac arrest provides values more indicative of the true cellular environment.
 |
lactate levels
Elevated arterial lactate levels are an early sensitive marker of tissue hypoperfusion, predicting both the severity of hemodynamic compromise and overall patient prognosis. Unlike the pH during cardiac arrest, interpreting a venous lactate level in relation to an arterial value could be useful in the workup and management of critically ill patients. Based on the available evidence, the correlation between arterial and venous lactate values appears to be quite close. A 1996 study by Younger of 48 emergency department patients in whom concurrent arterial and venous blood gas analyses were performed demonstrated that an abnormally elevated venous lactate level (1.6 mmol/L or greater) was 100% sensitive and 89% specific in predicting elevated arterial lactate levels. A 2000 study by Lavery bolstered these results, demonstrating a close correlation between arterial and venous lactate levels in a population of 375 hypovolemic trauma patients. A venous lactate level above 2 mmol/L predicted an elevated injury severity score, ICU admission, and length of stay.
The bottom line: Venous lactate levels are similar to those found in arterial samples. A normal venous lactate measurement predicts a normal arterial lactate reading, precluding the need to perform an arterial puncture.
METABOLIC CONDITIONS
Using ABG measurements and serum electrolyte levels, the emergency physician can perform the six steps involved in calculating mixed acid-base disturbances (see box below). Venous pH values can aid in the first step because they closely mirror arterial values for several metabolic conditions, including diabetic ketoacidosis (DKA) and uremia.
 |
A 1998 study by Brandenburg of emergency department patients with DKA found remarkably similar values for arterial and venous pH (mean arterial, 7.20; mean venous, 7.17). HCO3 levels are also very similar (mean arterial, 11.0 +/- 6.0 mmol/L; mean venous, 12.8 +/- 5.5 mmol/L). A 2003 study by Ma of DKA patients presenting to the emergency department corroborated these findings. More importantly, it examined the effect that knowing a patient’s ABG values had on the clinician’s diagnosis, treatment plan, and patient disposition. Rarely did it alter care in the emergency department.
Other forms of metabolic acidosis have been studied. A similar relationship has been found, for example, between arterial and venous measurements in patients with metabolic acidosis due to uremia. A 2000 study by Gokel of 100 uremic patients found a mean arterial pH of 7.17 +/- 0.14 compared to a mean venous pH of 7.13 +/- 0.14, and a mean arterial HCO3 of 10.13 +/- 4.26 mmol/L compared to a mean venous HCO3 of 11.86 +/- 4.23 mmol/L. Some caution is warranted in interpreting a high potassium level in a uremic patient obtained on an arterial or venous blood gas sample because the analyzer will not distinguish true hyperkalemia from pseudohyperkalemia due to a hemolyzed sample.
The six steps in calculating mixed acid-base abnormalities cannot be completed without knowing the patient’s arterial PCO2 level. Specifically, concomitant respiratory conditions cannot be excluded. Other metabolic disorders can still be detected, however, by using information obtained from the serum electrolytes—namely, the anion and delta gaps.
The anion gap is determined by subtracting the sum of the patient’s serum bicarbonate and chloride levels from the sodium level, or AG = Na – (HCO3 + Cl). It is not a true gap, but an indirect estimate of the amount of unmeasured serum anions, from which one can infer the presence of an acid causing the patient’s acid-base derangement. Anion gap values above 12 are generally considered positive and should prompt a specific workup to identify the etiology and direct appropriate treatment.
Delta gap refers to the principle that in an uncomplicated anion gap metabolic acidosis (AGMA), for every 1 mmol/L elevation in the anion gap, there should be a reflexive 1 mmol/L drop in the serum HCO3 level. Any deviation from this suggests a mixed acid-base disorder—either a combined metabolic acidosis/alkalosis or mixed anion gap and non-anion gap metabolic acidosis (NAGMA). There are several ways to calculate the delta gap. One commonly used method is: delta gap equals the change in the anion gap (from the normal of 12) minus the change in the serum bicarbonate (from the normal of 24), or DG = (AG – 12) – (24 – HCO3). When the delta gap is greater than 6, there is a combination of AGMA and metabolic alkalosis. When it is less than -6, there is a combination of AGMA and NAGMA.
RESPIRATORY ILLNESS
In physiologic terms, ABG composition reflects the relationship between ventilation and perfusion and thus is an important reflection of overall pulmonary function. In clinical practice, respiratory insufficiency can be broken down into two categories—namely, ventilatory failure (inadequate clearance of CO2, or hypercarbia) and oxygenation failure (inadequate plasma oxygenation, or hypoxemia). Arterial blood gas analysis has long been used to diagnose and quantify the severity of either or both of the above conditions in patients with apparent respiratory distress.
A close correlation between arterial and venous PCO2 that would decrease dependency on an ABG does not exist. However, a venous PCO2 value that predicts significant arterial hypercarbia might be useful. In a study published in 2002 by Kelly, a venous PCO2 level above 45 mm Hg predicted an arterial PCO2 above 50 mm Hg (the designated value for significant hypercarbia) with a sensitivity of 100% and specificity of 57%. In this study, a venous PCO2 value above 45 mm Hg detected all cases of significant arterial hypercarbia (negative predictive value, 100%) and reduced the requirement for arterial blood sampling in 41% of cases.
Venous PO2 values do not provide any significant reflection of arterial PO2 levels and are therefore a poor surrogate to quantify oxygen delivery to target tissues. However, the widespread availability of pulse oximetry makes it an attractive alternative. A 2001 study by Witting of more than 700 emergency department patients showed that an oxygen saturation level of 96% or less on room air predicted a PO2 below 70 mm Hg with a sensitivity of 100% and a specificity of 54%.
CASE RESOLUTION
With the conclusions from the various studies cited above in mind, you tell the nurse to add a VBG to the rest of the labs and you hold off on an ABG analysis. Within two minutes, the results of the VBG return: pH, 7.12; PCO2, 27; PO2, 27; HCO3, 9, and lactate, 1.2. The nurse notifies you that the urine dipstick test is positive for ketones.
You begin treating the patient with fluids and insulin for presumed DKA based on the elevated serum glucose level, urine dipstick test, and VBG results showing a low pH and a low HCO3 consistent with a metabolic acidosis. Forty minutes later, the chemistries come back and confirm an AGMA (sodium, 129; chloride, 101; potassium, 7.3; HCO3, 9; blood urea nitrogen, 55; creatinine, 3.0; glucose, 686; anion gap, 19). The decision is made to admit the patient to the hospital, but the floor resident accepting the patient calls down and requests that you perform an ABG. You know you have not ruled out a mixed acid-base disorder, but you can’t remember the last time you calculated it or changed your management based on it. Nonetheless, you decide to calculate a delta gap based on the chemistry results as follows: DG = [(AG-12) – (24 – HCO3)] = [(19 – 12) – (24 – 9)] = (7 – 15) = -8. Given a delta gap of less than -6, you diagnose an additional metabolic derangement—an NAGMA.
Your thoughts next turn to the possibility that a significant respiratory disorder may be present. The patient is tachypneic, but this may be due to his acidosis. Knowing that a venous PCO2 below 45 mm Hg indicates an arterial PCO2 below 50 mm Hg, you feel confident that significant hypercarbia in this patient is unlikely given his venous PCO2 of 27 mm Hg. Additionally, the patient’s pulse oximeter shows an oxygen saturation of 97%, and you conclude that there is no significant hypoxia (PO2 above 70 mm Hg).
The patient is admitted to the hospital, where the insulin drip is continued. His symptoms improve and his anion gap closes. He is discharged two days later without an ABG analysis having been performed.
| Suggested Reading Abramson D, et al.: Lactate clearance and survival following injury. J Trauma 35(4):584, 1993. Adrogue HJ, et al.: Assessing acid-base status in circulatory failure: differences between arterial and central venous blood. N Engl J Med 320(20):1312, 1989. Boontje AH: Latrogenic arterial injuries. J Cardiovasc Surg (Torino) 19(4):335, 1978. Brandenburg MA and Dire DJ: Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis. Ann Emerg Med 31(4):459, 1998. Gambino SR: Normal values for adult human venous plasma pH and CO2 content. Tech Bull Regist Med Technol 29:132, 1959. Gennis PR, et al.: The usefulness of peripheral venous blood in estimating acid-base status in acutely ill patients. Ann Emerg Med 14(9):845, 1985. Giner J, et al.: Pain during arterial puncture. Chest 110(6):1443, 1996. Gokel Y, et al.: Comparison of blood gas and acid-base measurements in arterial and venous blood samples in patients with uremic acidosis and diabetic ketoacidosis in the emergency room. Am J Nephrol 20(4):319, 2000. Griffith KK, et al.: Mixed venous blood-gas composition in experimentally induced acid-base disturbances. Heart Lung 12(6):1983. Johnston HL and Murphy R: Agreement between an arterial blood gas analyser and a venous blood analyser in the measurement of potassium in patients in cardiac arrest. Emerg Med J 22(4):269, 2005. Kelly AM, et al.: Venous pCO(2) and pH can be used to screen for significant hypercarbia in emergency patients with acute respiratory disease. J Emerg Med 22(1):15, 2002. Lavery RF, et al.: The utility of venous lactate to triage injured patients in the trauma center. J Am Coll Surg 190(6):656, 2000. Ma OJ, et al.: Arterial blood gas results rarely influence emergency physician management of patients with suspected ketoacidosis. Acad Emerg Med 10(8):836, 2003. Mizock BA and Falk JL: Lactic acidosis in critical illness. Crit Care Med 20(1):80, 1992. Morganroth ML: An analytic approach to diagnosing acid-base disorders. J Crit Illn 5(2):138, 1990. Morganroth ML: Six steps to acid-base analysis: clinical applications. J Crit Illn 5(5):460, 1990. Nguyen HB, et al.: Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 32(8):1637, 2004. Rutecki GW and Whittier FC: An approach to clinical acid-base problem solving. Compr Ther 24(11-12):553, 1998. Weil MH, et al.: Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med 315(3):153, 1986. Wilson M, et al.: Diagnosis and monitoring of hemorrhagic shock during the initial resuscitation of multiple trauma patients: a review. J Emerg Med 24(4):413, 2003. Witting MD and Lueck CH: The ability of pulse oximetry to screen for hypoxemia and hypercapnia in patients breathing room air. J Emerg Med 20(4):341, 2001. Wrenn K: The delta (delta) gap: an approach to mixed acid-base disorders. Ann Emerg Med 19(11):1310, 1990. Younger JG, et al.: Relationship between arterial and peripheral venous lactate levels. Acad Emerg Med 3(7):730, 1996. |
Source:http://www.ncemi.org/cse/cse0313.htm
Presentation
The patient thinks he recently swallowed a fish or a chicken bone, pop top from an old-style can, or something of the sort, and still can feel a foreign body sensation in his throat, especially (perhaps painfully) when swallowing. He may be convinced that there is a bone or other object stuck in the throat. He may be able to localize the foreign body sensation precisely above the thyroid cartilage (implying a foreign body in the hypopharynx you may be able to see), or he may only vaguely localize the foreign body sensation to the suprasternal notch (which could imply an foreign body anywhere in the esophagus). A foreign body in the tracheobronchial tree usually stimulates coughing and wheezing. Obstruction of the esophagus produces drooling and spitting up of whatever fluid is swallowed.
An intussusception is a medical condition in which a part of the intestine has invaginated into another section of intestine, similar to the way in which the parts of a collapsible telescope slide into one another.[1] This can often result in an obstruction. The part that prolapses into the other is called the intussusceptum, and the part that receives it is called the intussuscipiens.
Symptoms
Early symptoms can include nausea, vomiting - sometimes bile stained (green color), pulling legs to the chest area, and intermittent moderate to severe cramping abdominal pain. Pain is intermittent not because the intussusception temporarily resolves, but because the intussuscepted bowel segment transiently stops contracting. Later signs include rectal bleeding, often with 'red currant jelly' stool (stool mixed with blood and mucus), and lethargy. Physical examination may reveal a 'sausage-shaped' mass felt upon palpation of the abdomen.
CASE:
A 50-year-old man presents for evaluation of a lesion on the lateral canthus of his left eye. Recently, the lesion has started to bleed. The patient insists that the growth has been present since birth or early childhood and that it began to slowly increase in size throughout the past year. Family history is negative for skin cancer. Examination reveals a 1.2-cm reddish nodule with telangiectasias and central denudation. A biopsy is performed, and the patient is urged to check photographs from his youth to verify that the lesion was present during his childhood.
WHAT IS YOUR DIAGNOSIS?
Cramps are unpleasant, often painful sensations caused by muscle contraction or overshortening. The common causes of skeletal muscle cramps are muscle fatigue and a sodium imbalance. Smooth muscle cramps may be due to menstruation or Gastroenteritis.
Differential diagnosis
Causes of cramping include hyperflexion, hypoxia, exposure to large changes in temperature, dehydration, or low blood salt. Muscle cramps may also be a symptom or complication of pregnancy, kidney disease, thyroid disease, hypokalemia, or hypocalcemia (as conditions), restless-leg syndrome, varicose veins, and multiple sclerosis.
A hiccup or hiccough (pronounced /ˈhɪkʌp/ HICK-up) is a contraction of the diaphragm that repeats several times per minute. In humans, the abrupt rush of air into the lungs causes the epiglottis to close, creating a "hic" sound.
In medicine it is known as synchronous diaphragmatic flutter (SDF), or singultus, from the Latin singult, "the act of catching one's breath while sobbing".The hiccup is an involuntary action involving a reflex arc.
A bout of hiccups, in general, resolves itself without intervention, although many home remedies claim to shorten the duration, and medical treatment is occasionally necessary in cases of chronic hiccups.
© Blogger templates Newspaper III by Ourblogtemplates.com 2008
Back to TOP
