pneumothorax
1) spontaneous: bleb rupture
2) tension: penetrating
flail chest >= 4 ribs broken
cardiac tamponade = knife wound left chest
Beck's triad
hypotension
JVD(jugular vein distension)
muffled heart sound
VAN = vein, artery, nerve, below the ribs
Pericardiocentesis, do it above the rib because VAN below the rib
APKD (adult polycistic kidney disease) and its association with Berry's aneurysm(type of cerebral aneurysm)
Appendicitis
-signs
- Obturator sign
- Psoas sign
- Rovsing's sign
- Valentino's sign
- McBurney's point
- Yersinia enterocolitis mimics appendicitis
Pancrease = beta cell insulin -> hypoglycemic
glucagon = hyperglycemic
endocrine
exocrine
Diabetes type I = insulin + K+
type II = oral hyperglycemia (receptor defect)
ATN(acute tubular necrosis)
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In medicine (pulmonology), a pneumothorax or collapsed lung is a medical emergency caused by the collapse of the lung within the pleural cavity.
It can result from:
- A penetrating chest wound
- Barotrauma to the lungs
- Spontaneously (most commonly in tall slim young males and in Marfan syndrome)
- Chronic lung pathologies including emphysema, asthma
- Acute infections
- Chronic infections, such as tuberculosis
- Cancer
- Catamenial pneumothorax (due to endometriosis in the chest cavity)
Pneumothoraces are divided into tension and non-tension pneumathoraces. A tension pneumathorax is a medical emergency as air accumulates in the pleural space with each breath. The remorseless increase in intrathoracic pressure results in massive shifts of the mediastinum away from the affected lung compressing intrathoracic vessels. A non-tension pneumothorax by contrast is a less severe pathology because the air in the pneumothorax is able to escape.
The accumulation of blood in the thoracic cavity (hemothorax) exacerbates the problem, creating a pneumohemothorax.
Signs and symptoms
Sudden shortness of breath, cyanosis (turning blue) and pain felt in the chest and/or back are the main symptoms. In penetrating chest wounds, the sound of air flowing through the puncture hole may indicate pneumothorax, hence the term "sucking" chest wound. The flopping sound of the punctured lung is also occasionally heard.
If untreated, hypoxia may lead to loss of consciousness and coma. In addition, shifting of the mediastinum away from the site of the injury can obstruct the superior and inferior vena cava resulting in reduced cardiac preload and decreased cardiac output. Untreated, a severe pneumothorax can lead to death within several minutes.
Spontaneous pneumothoraces are reported in young people with a tall stature. As men are generally taller than women, there is a preponderance among males. The reason for this association, while unknown, is hypothesized to be the presence of subtle abnormalities in connective tissue.
Pathophysiology
The lungs are located inside the chest cavity, which is a hollow space. Air is drawn into the lungs by the diaphragm (a powerful abdominal muscle). The pleural cavity is the region between the chest wall and the lungs. If air enters the pleural cavity, either from the outside (open pneumothorax) or from the lung (closed pneumothorax), the lung collapses and it becomes mechanically impossible for the injured person to breathe, even with an open airway. If a piece of tissue forms a one-way valve that allows air to enter the pleural cavity from the lung but not to escape, overpressure can build up with every breath; this is known as tension pneumothorax. It may lead to severe shortness of breath as well as circulatory collapse, both life-threatening conditions. This condition requires urgent intervention.
A tension pneumothorax is a life-threatening condition that results from a progressive deterioration and worsening of a simple pneumothorax, associated with the formation of a one-way valve at the point of rupture.[1]
Upon inspiration, when the pressure inside the chest and pleural cavity lessens as a result of the respiratory muscles increasing chest dimensions, air is sucked in through this one way valve, into the pleural space. Because expiration is a passive process, there is an insignificant amount of pressure created to force the air back out of the pleural cavity. This condition over time results in a gradual accumulation of air to the degree that it begins to put pressure on the mediastinum, compressing the heart and decreasing cardiac output due to the reduced amount of diastolic filling of the ventricles, and also putting pressure against the trachea, deviating it from the midline. Because of the increased thoracic pressure, venous return to the heart is decreased, causing a backup of blood into the venous system, as is evidence by distended jugular veins.[1]
Differentiation
A tension pneumothorax is a condition whose signs and symptoms resemble very closely those of a condition called pericardial tamponade. A chest x-ray will distinguish the two. On physical exam, the differentiating factors are:
- Pericardial tamponade
- Breath sounds: Equal on both sides
- Trachea: Midline
- Percussion: Normal resonance
- Pulse: Affected by breathing, called pulsus paradoxus, or simply paradoxical pulse.
- Tension pneumothorax
- Breath sounds: Decreased or absent on affected side
- Trachea: Deviated to unaffected side
- Percussion: Hyper-resonance
- Pulse: Normal
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Main Entry: bleb
Pronunciation: 
bleb
Function: noun
1 : a small blister -- compare BULLA 2
2 : something resembling a bleb; especially : a vesicular outpocketing of a plasma or nuclear membrane
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Beck's triad is comprised of fall in the systolic pressure, rising jugular venous pressure and suppressed heart sounds. These findings are typical of cardiac tamponade.
1: The rising jugular venous pressure is evidenced by distended jugular veins while in a non-supine position. It is caused by reduced diastolic filling of the right ventricle, due to the outside pressure being exerted on it by the expanding pericardial sac. This results of a backup of fluid into the veins draining into the heart, most notably, the jugulars. In severe hypovolaemia, the neck veins may NOT be distended.
2: The fall in systolic pressure results when the fluid in the pericardial cavity accumulates to a degree that it impairs ventricular stretch, thus reducing stroke volume and cardiac output.
3: The suppressed heart sounds occur due to the muffling effects of the sounds passing through the fluid surrounding the heart.
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Pleural effusion is excess fluid that accumulates in the pleural cavity, the fluid-filled space that surrounds the lungs.
Four types of fluids can accumulate in the pleural space:
- Serous fluid (hydrothorax)
- Blood (hemothorax)
- Chyle (chylothorax)
- Pus (pyothorax or empyema)
Pathophysiology
Healthy individuals have less than 1 ml of fluid in each pleural space. Normally, fluid enters the pleural space from the capillaries in the parietal pleura, from interstitial spaces of the lung via the visceral pleura, or from the peritoneal cavity through small holes in the diaphragm. This fluid is normally removed by lymphatics in the parietal pleura, which have the capacity to absorb 20 times more fluid than is normally formed. When this capacity is overwhelmed, either through excess formation or decreased lymphatic absorption, a pleural effusion develops.
[edit] Diagnosis
Pleural effusion is usually diagnosed on the basis of the history and physical exam, and confirmed by chest x-ray. Chest films acquired in the lateral decubitus position (with the patient lying on their side) are more sensitive, and can pick up as little as 50 ml of fluid. At least 300 ml of fluid must be present before upright chest films can pick up signs of pleural effusion (e.g., blunted costophrenic angles). Once accumulated fluid is more than 500 ml, there are usually detectable clinical signs in the patient, such as decreased movement of the chest on the affected side, dullness to percussion over the fluid, diminished breath sounds on the affected side, decreased vocal fremitus and resonance, pleural friction rub, and egophony.
Once a pleural effusion is diagnosed, the cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis. A needle is inserted through the back of the chest wall into the pleural space. The fluid may then be evaluated for the following:
- Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH and glucose
- Gram stain and culture to identifies bacterial infections
- Cell count and differential
- Cytology to identify cancer cells, but may also identify some infective organisms
- Other tests as suggested by the clinical situation - lipids, fungal culture, viral culture, specific immunoglobulins
[edit] Transudate vs. exudate
The first step in the evaluation of pleural fluid is to determine whether the effusion is a transudate or an exudate. Transudative pleural effusions are caused by systemic factors that alter the balance of the formation and absorption of pleural fluid (e.g., left ventricular failure, pulmonary embolism, and cirrhosis), while exudative pleural effusions are caused by alterations in local factors that influence the formation and absorption of pleural fluid (e.g., bacterial pneumonia, cancer, viral infection, and pulmonary embolism).
[edit] Light's criteria
Transudative and exudative pleural effusions are differentiated by comparing protein and lactate dehydrogenase levels in the pleural fluid to those in the blood. Exudative pleural effusions meet at least one of the following criteria (Light's criteria), whereas transudative pleural effusions meet none:
- The ratio of pleural fluid protein to serum protein is greater than 0.5
- The ratio of pleural fluid LDH and serum LDH is greater than 0.6
- Pleural fluid LDH is more than two-thirds normal upper limit for serum
Twenty-five percent of patients with transudative pleural effusions are mistakenly identified as having exudative pleural effusions by Light's criteria. Therefore, additional testing is needed if a patient identified as having an exudative pleural effusion appears clinically to have a condition that produces a transudative effusion. In such cases albumin levels in blood and pleural fluid are measured. If the difference between the albumin levels in the blood and the pleural fluid is greater than 1.2 g/dL (12 g/L), it can be assumed that the patient has a transudative pleural effusion.
If the fluid is definitively identified as exudative, additional testing is necessary to determine the local factors causing the exudate.
[edit] Exudative pleural effusions
Once identified as exudative, additional evaluation is needed to determine the cause of the excess fluid, and pleural fluid amylase, glucose, and cell counts are obtained. The fluid is also sent for Gram staining and culture, and, if suspicious for tuberculosis, examination for TB markers (adenosine deaminase > 45 IU/L, interferon gamma > 140 pg/mL, or positive polymerase chain reaction (PCR) for tuberculous DNA).
Pleural fluid amylase is elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer. Glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis. If cancer is suspected, the pleural fluid is sent for cytology. If cytology is negative, and cancer is still suspected, either a thoracoscopy, or needle biopsy of the pleura may be performed.
[edit] Causes
The most common causes of transudative pleural effusions in the United States are left ventricular failure, pulmonary embolism, and cirrhosis (causing hepatic hydrothorax), while the most common causes of exudative pleural effusions are bacterial pneumonia, cancer (with lung cancer, breast cancer, and lymphoma causing approximately 75% of all malignant pleural effusions), viral infection, and pulmonary embolism. Although pulmonary embolism can produce either transudative or exudative pleural effusions, the latter is more common.
Other causes of pleural effusion include, tuberculosis (though pleural fluid smears are rarely positive for AFB, this is the most common cause of pleural effusion in some developing countries), autoimmune disease such as systemic lupus erythematosus, bleeding (often due to chest trauma), chylothorax (most commonly caused by trauma), and accidental infusion of fluids. Less common causes include, esophageal rupture or pancreatic disease, intraabdominal abscess, rheumatoid arthritis, asbestos pleural effusion, Meig's syndrome (ascites and pleural effusion due to a benign ovarian tumor), and ovarian hyperstimulation syndrome.
Pleural effusions may also occur through medical/surgical interventions, including the use of medications (pleural fluid is usually eosinophilic), coronary artery bypass surgery, abdominal surgery, endoscopic variceal sclerotherapy, radiation therapy, liver or lung transplantation, and intra- or extravascular insertion of central lines.
[edit] Treatment
Treatment depends on the underlying cause of the pleural effusion. Therapeutic aspiration may be sufficient; larger effusions may require insertion of an intercostal drain (either pigtail or surgical). Repeated effusions may require chemical (talc, bleomycin, tetracycline/doxycycline) or surgical pleurodesis, in which the two pleural surfaces are attached to each other so that no fluid can accumulate between them.
--------------------------------------------------------------------------A flail chest occurs when a segment of the thoracic wall breaks under extreme stress and becomes detached from the rest of the chest wall. It is a serious chest injury often associated with underlying pulmonary injury.
This typically occurs when a three or more ribs are fractured in two or more places, allowing that segment of the thoracic wall to displace and move independently of the rest of the chest wall. Flail chest can also occur when ribs are fractured proximally in conjunction with disarticulation of costochondral cartilages distally.
The characteristic paradoxical motion of the flail segment occurs due to pressure changes associated with respiration that the rib cage normally resists:
- During inspiration, the diaphragm contracts and intercostal muscles push the rib cage out. Pressure in the thorax decreases below atmospheric pressure, and air rushes in through the trachea. However, a flail segment will not resist the decreased pressure and will appear to push in while the rest of the rib cage expands.
- During expiration, the diaphragm and intercostal muscles relax, allowing the abdominal organs to push air upwards and out of the thorax. However, a flail segment will also be pushed out while the rest of the rib cage contracts.
The constant motion of the ribs in the flail segment at the site of the fracture is exquisitely painful, and the sharp broken edges of the ribs are likely to eventually puncture the pleural sac and lung, which may be fatal.
[edit] Treatment
Treatment of the flail chest initially follows the principles of Advanced Trauma Life Support, further treatment includes:
- Good analgesia including intercostal blocks, avoiding narcotic analgesics as much as possible. This allows much better ventilation, with improved tidal volume, and increased blood oxygenation.
- Positive ventilation, meticulosly adjusting the ventilator settings to avoid barotrauma.
- Surgical fixation is usually not required.
- Chest tubes as required.
Appendicitis (or epityphlitis) is a condition characterised by inflammation of the appendix. While mild cases may resolve without treatment, most require removal of the inflamed appendix, either by laparotomy or laparoscopy. Untreated, mortality is high, mainly due to peritonitis and shock.
Causes
The causes of appendicitis are generally unknown, but the leading theory is that obstruction of the appendiceal orifice is the inciting factor. Obstruction may come from fecal matter lodged in the appendix, impaction of mucous, a small tumor (such as a carcinoid), or even a small blood clot. Populations with high fiber diets have a low incidence of appendicitis and diverticulitis leading some to conclude diet induced constipation is a contributing cause. Viral infections, which can cause ulceration of the lining, can also lead to obstruction of the appendix through proliferation of lymphatic tissue in its walls. A viral etiology is a possible explanation for seasonal variations in rates of appendicitis and clustering of cases. Regardless of the cause, obstruction of the appendix may lead to progressive appendiceal distension. This distension increases the pressure within the appendix, which in turn impairs its blood supply. Deprived of blood, the appendix loses the ability to fight infection and fecal bacteria begin to grow out of control. Although spontaneous recovery can rarely occur, with time and lack of treatment the walls of the appendix eventually become gangrenous from the infection and lack of blood flow. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result of this cascade is appendiceal rupture causing peritonitis, which may lead to septicemia and eventually death.
Although the model described above is traditionally taught in medical schools, histories of patients operated for appendicitis do not often correlate well with such a single disease progression. Specifically, those with atypical histories have findings at surgery that are consistent with a suppurative process that starts at the onset of symptoms and then smolders. Patients with typical histories may have findings suggesting resolution. Histories to suggest rupture of the appendix while patients are being diagnostically observed are exceedingly rare.
Thus appendicitis is now considered by some to behave as two distinct disease processes, typical and atypical (or suppurative). Approximately two-thirds of patients with appendicitis have typical histories, and findings suggest a virus or mild obstruction as a cause. In the third with atypical histories, an early suppurative process begins at the clinical onset, and severe unremitting obstruction is the likely cause. In any case, early surgical removal is the best treatment for either type of appendicitis. (Hobler,K., 1998)
Appendicitis’ apparently idiopathic nature has led to many different theories explaining its occurrence. One theory regarding the cause of appendicitis, sometimes facetiously referred to as "the porcelain throne theory”, was proposed by Dr. Denis Burkitt, who developed the theory after observing low rates of appendicitis in Uganda. He proposed two causes for this: one, the Africans ate a diet high in fiber, and two, they used squat toilets rather than seat toilets. Most health practitioners accept Dr. Burkitt's first cause as a contributing factor, but are unfamiliar with the second one, which has never been tested.
A third hypothesis, which has gained less attention, proposes that a lack of adequate sanitary facilities in the developing world may actually have a protective effect against later appendicitis. This theory, proposed by Baker in 1985, hypothesized that infants in the developed world are exposed to fewer enteric organisms, which modifies their immune response to virus infections, which might then cause appendicitis. This is also unverified. [1]
[edit] Signs, symptoms and findings
Appendicitis can be classified into two types, typical and atypical. The pain of typical acute appendicitis usually starts centrally (periumbilical) before localising to the right iliac fossa (the lower right side of the abdomen). There is usually associated loss of appetite (anorexia) and fever. Nausea, or vomiting may or may not occur. These classic signs and symptoms are more likely the younger the patient. Older patients (beyond their teenage years) may present with only one or two. Diagnosis is easier in typical acute appendicitis and surgery removes a swollen appendix with little or no suppuration (pus) if operated early (within 24 hours of onset).
Atypical histories are not unusual and are more often associated with suppurative appendicitis. This condition often starts with right lower quadrant pain and may smolder for several days before a diagnosis of appendicitis can be made. Diagnosis is more difficult and surgery removes an appendix that is suppurative, gangrenous or ruptured.
There is typically pain and tenderness in the right iliac fossa in both typical and atypical (suppurative) appendicitis. Rebound tenderness may be present suggesting that there is some element of peritoneal irritation. If the abdomen is involuntarily guarded, there should be a strong suspicion of peritonitis requiring urgent surgical intervention.
[edit] Diagnosis
Diagnosis is based on history and physical examination backed by an elevation of neutrophilic white cells, and other infection markers on blood testing and imaging.
The classical history in appendicitis is diffuse pain in the periumbilical region which then localizes as pain and tenderness at McBurney's point (associated with an inflamed appendix coming in contact with the surrounding parietal peritoneum). This point is located on the right-hand side of the abdomen one-third of the distance between the anterior superior iliac spine and the navel. Here, on gentle palpation, the abdominal muscles often feel firm to rigid because of involuntary spasm, and a cough also produces a localized soreness.
Other physical findings include right-side tenderness on a digital rectal exam. Since the appendix normally lies on the right, if a finger is inserted into the rectum and there is tenderness when pressure is applied toward the right, this indicates an increased likelihood that the patient has appendicitis.
Other signs used in the diagnosis of appendicitis are the psoas sign (useful in retrocecal appendicitis), the obturator sign (specifically the obturator internus muscle), Blumberg's sign, and Rovsing's sign.
Ultrasonography and Doppler sonography also provide useful means to detect appendicitis, especially in children. In some cases (15% approximately), however, ultrasonography of the iliac fossa does not reveal any abnormalities despite the presence of appendicitis. This is especially true of early appendicitis before the appendix has become significantly distended and in adults where larger amounts of fat and bowel gas make actually seeing the appendix technically difficult. Despite these limitations, in experienced hands sonographic imaging can often distinguish between appendicitis and other diseases with very similar symptoms such as inflammation of lymph nodes near the appendix or pain originating from other pelvic organs such as the ovaries or fallopian tubes.
In places where it is readily available, CT scan has become the diagnostic test of choice, especially in adults. A properly performed CT scan with modern equipment has a detection rate (sensitivity) of over 95% and a similar specificity. Signs of appendicitis on CT scan include lack of contrast (oral dye) in the appendix and direct visualization of appendiceal enlargement (greater than 6 mm in diameter on cross section). The inflammation caused by appendicitis in the surrounding peritoneal fat (so called "fat stranding") can also be observed on CT, providing a mechanism to detect early appendicitis and a clue that appendicitis may be present even when the appendix is not well seen. Thus, diagnosis of appendicitis by CT is made more difficult in very thin patients and in children, both of whom tend to lack significant fat within the abdomen. In most cases, however, appendicitis is a clinical diagnosis and, due to the high radiation dose involved, CT scans are only used when the diagnosis is in doubt (e.g. atypical history) or if there are other considerations involved.
[edit] Treatment
Appendicitis can be treated by removal of the appendix through a surgical procedure called an appendicectomy (also known as an appendectomy). The incision of appendectomy can be a Gridiron incision, a Lanz incision, or the midline incision.
Often now the operation can be performed via a laparoscopic approach, or via small incisions with a camera to visualize the area of interest in the abdomen. If the findings reveal suppurative appendicitis with complications such as rupture, abscess, adhesions, etc., conversion to open laparotomy may be necessary.
Antibiotics are often given intravenously to help kill remaining bacteria and thus reduce the incidence of infectious complication in the abdomen or wound.
[edit] Prognosis
Most appendicitis patients recover easily with treatment, but complications can occur if treatment is delayed or if peritonitis occurs.
Recovery time depends on age, condition, complications, and other circumstances but usually is between 10 and 28 days.
The real possibility of life-threatening peritonitis is the reason why acute appendicitis warrants speedy evaluation and treatment. The patient may have to undergo a medical evacuation. Appendectomies have occasionally been performed in emergency conditions (i.e. outside of a proper hospital), when a timely medical evacuation was impossible.
Typical acute appendicitis responds quickly to appendectomy and occasionally will resolve spontaneously. If appendicitis resolves spontaneously, it remains controversial whether an elective interval appendectomy should be performed to prevent a recurrent episode of appendicitis. Atypical appendicitis (associated with suppurative appendicitis) is more difficult to diagnose and is more apt to be complicated even when operated early. In either condition prompt diagnosis and appendectomy yield the best results with full recovery in two to four weeks usually. Mortality and severe complications are unusual but do occur, especially if peritonitis persists untreated.
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Signs of appendicitis
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The obturator sign is an indicator of irritation to the obturator internus muscle.
In the clinical context, it is performed when acute appendicitis is suspected. In this condition, the appendix becomes inflamed and enlarged. The appendix may come into physical contact with the obturator internus muscle, which will be stretched by this physical examination maneuver. This causes pain and is an evidence in support of an inflamed appendix.
The principles of the obturator sign in the diagnosis of appendicitis are similar to the psoas sign.
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Elicited by the iliopsoas test, the psoas sign is an indicator of irritation to the iliopsoas group of hip flexors in the abdomen.
The test is performed by having a supine patient with knees extended flex their thighs against resistance. If abdominal pain results, it is a positive psoas sign. [1]
Because the right iliopsoas muscle lies under the appendix when the patient is supine, a "positive psoas sign" may suggest appendicitis.
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Rovsing's sign is a sign of appendicitis. If palpation of the lower left quadrant of a person's abdomen results in more pain in the right lower quadrant, the patient is said to have a positive Rovsing's sign and may have appendicitis.
This anomaly occurs because the pain nerves deep in the intestines do not localize well to an exact spot on the abdominal wall, unlike pain nerves in muscles. Pain from a stomach ulcer or gallstone can be interpreted by the brain as pain from the stomach, liver, gall bladder, duodenum, or first part of the small intestine. It will "refer" pain often to the mid upper abdomen.
Because the appendix is a piece of intestine, it follows a similar referral pattern. An appendix with some early inflammation may give a non-specific irritation somewhere near the umbilicus (belly button). Should the inflammation become severe, it may actually irritate the inner lining of the abdominal cavity called the peritoneum. This thin layer lies under or behind the abdominal wall muscles. Now the pain is "localized". If pressure is applied to the muscles of the right lower abdomen (or iliac fossa) near a very irritated appendix , then the muscle fibers in that area will be stretched and will hurt.
A Rosving's sign is elicited by pushing on the abdomen far away from the appendix which, on most people, is in the right lower quadrant. While this maneuver stretches the entire peritoneal lining, it only causes pain in any location where peritoneum is irritating the muscle. In the case of appendicitis, the pain is felt in the right lower quadrant despite pressure being placed elsewhere.
Most practitioners push on the left lower quadrant to see where the patient complains of pain. If pain is felt in the right lower quadrant, then there may be an inflamed organ or piece of tissue in the right lower quadrant. The appendix is generally the prime suspect, although other pathology can also give a "positive" Rosving's sign. If left lower quadrant pressure by the examiner leads only to left-sided pain or pain on both the left and right sides, then there may be some other pathologic etiology. This may include causes relating to the bladder, uterus, descending (left) colon, fallopian tubes, ovaries, or other structures.
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McBurney's point is the name given to the point over the right side of the human abdomen that is one-third of the distance from the ASIS (anterior superior iliac spine) to the umbilicus. This point roughly corresponds to the most common location of the base of the appendix where it is attached to the cecum.
[edit] Clinical relevance
Deep tenderness at McBurney's point, known as McBurney's sign, is a sign of acute appendicitis. The clinical sign of rebound pain when pressure is applied is also known as Aaron sign.
Specific localization of tenderness to McBurney's point indicates that inflammation is no longer limited to the lumen of the bowel (which localizes pain poorly), and is irritating the lining of the peritoneum at the place where the peritoneum comes into contact with the appendix. Tenderness at McBurney's point suggests the evolution of acute appendicitis to a later stage, and thus, the increased likelihood of rupture. Because the location of the appendix is often different in different people, and can migrate within the abdomen, many cases of appendicitis do not cause point tenderness at McBurney's point. Other abdominal processes can also sometimes cause tenderness at McBurney's point. Thus, this sign is highly useful but neither necessary nor sufficient to make a diagnosis of acute appendicitis. Also, the anatomical position of the appendix is highly variable (for example in retrocaecal appendix, an appendix behind the caecum), which also limits the use of this sign.
--------------------------------------------------------------------------Acute tubular necrosis or (ATN) is a medical condition involving the death of tubular cells that form the tubule that transports urine to the ureters while reabsorbing 99% of the water (and highly concentrating the salts and metabolic byproducts). Tubular cells continually replace themselves and if the cause of ATN is removed then recovery is likely. ATN presents with acute renal failure to the point that the two concepts are used interchangeably.
It may be classified as either toxic or ischemic. Toxic ATN occurs when the tubular cells are exposed to a toxic substance (nephrotoxic ATN). Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition they are highly senistive to due to their very high metabolism.
Toxic ATN
Toxic ATN can be caused by free hemoglobin or myoglobin, by medication such as antibiotics and cytostatic drugs, or by intoxication (ethylene glycol, "anti-freeze").
Histopathology: Toxic ATN is characterized by proximal tubular epithelium necrosis (no nuclei, intense eosinophilic homogeneous cytoplasm, but preserved shape) due to a toxic substance (poisons, organic solvents, drugs, heavy metals). Necrotic cells fall into the tubule lumen, obliterating it, and determining acute renal failure. Basement membrane is intact, so the tubular epithelium regeneration is possible. Glomeruli are not affected.
[edit] Ischemic ATN
Ischemic ATN can be caused when the kidneys are not sufficiently perfused for a long period of time (i.e. renal artery stenosis) or during shock. Hypoperfusion can also be caused by embolism of the renal arteries. Ischemic ATN specifically causes skip lesions through the tubules.
