EVOLUTION OF CHOLANGITIS
It can be positive and transient, moving so regressive, either spontaneously or under treatment.
But this favorable access without prejudice to the subsequent development, the appearance of recurrences may themselves give rise rapidly to serious complications, will indeed be based on the persistence or not of the obstacle and causal nature of the obstacle.
COMPLICATIONS
Early complications
Complications related to the onset of sepsis:
Gram-negative sepsis
Sepsis is characterized by significant and repeated shocks in the blood of pathogens from an outbreak of some kind.
Sepsis is likely to cause secondary outbreaks that will multiply more or less apparent.
Clinically it results:
* High fever which is the presence of bacteria in large numbers in the blood.
* Drop in blood pressure.
* Face greyish.
* Cold extremities.
* Tachycardia.
* Signs indicating a disorder of blood coagulation.
* Chills, asthenia.
* Malaysia, Splenomegaly.
* Difficulty breathing.
The diagnosis is confirmed by the laboratory through which a blood culture and determination of an effective antibiotic (for sensitivity) is made at the time of fever spikes. The appearance of multiple visceral involvement, has in some cases to confirm the clinical diagnosis.Finally, a septic shock endotoxin may be, with:
* Events kidney.
* Cardiovascular collapse.
* Hemorrhagic Syndrome.
* Centro lobular hepatic necrosis.
* Acute edematous pancreatitis or nérotico colitis.
The renal manifestations
Encompasses a range of syndrome of varying severity, ranging from simple functional renal failure in renal organic. These renal failure occur more readily in subjects with multiple defects, and those with a long history of bladder.
Clinically: it generally does not change the little picture of cholangitis:
* Jaundice, however, can change the type and take a look flamboyant.
* Hypotension is common.
Own signs of kidney disease (anorexia, nausea, vomiting, drowsiness, impaired consciousness), are difficult to distinguish from those of cholangitis.
In practice, it should be distinguished:
The benign forms: usually corresponding to functional renal failure with oliguria, urinary urea concentration is high, but creatinine is normal. They cause dehydration with hydro electrolytic disorders, but are reversible after fluid replacement and / or hydro electrolytic rebalancing.
Serious: with oligo anuria, diuresis or retained, but with azotemia and creatinine still high, and the significant decrease in urinary urea concentration.The cardiovascular collapse
Installation is quick and brutal, manifested clinically by:
- A fall in blood pressure.
- Tachycardia.
- A fast breathing.
- A fall in central venous pressure.
- Oliguria.
Sometimes profuse diarrhea and vomiting sometimes bleeding.
The hemorrhagic syndrome
With mucocutaneous bleeding, or hematemesis, or melena alone. GI bleeding in this case, is often related to stress peptic ulcers, the occurrence of disseminated intravenous coagulation aggravates the bleeding.
Loco regional complications
Extension of the inflammatory process and infection with various elements of the hepatic pedicle:Relatively frequent local complications (20% of cases), may pose difficult surgical problems, pédiculite this is seen especially in patients subjected to prolonged antibiotic therapy, for which the time of surgery was delayed.
Liver abscesses:Are the result of direct spread of infection, but may be the result of localization of metastatic sepsis.
Miliary abscesses:Are the most frequent single abscess is rarer, likely to surgical drainage.
Pédiculites and abscesses:Can cause internal fistula generally, and perforations in the peritoneum free or partitioned, they are difficult to diagnose.
Late Complications
Sclerosing cholangitis and secondary
They are usually defined as disorders of the biliary tract acquired, non-tumor, diffuse or multifocal. They are generally characterized by irregularities in caliber of the bile duct strictures and dilatations involving. The inflammatory and sclerosing character is more often inferred from the radiological appearance as shown by histological examination.
The secondary cholangitis should be distinguished from a primary sclerosing cholangitis, and other aspects of irregular bile ducts caused by a tumor, or a breach of the light of the bile ducts more than that of their wall.
Clinically it results:
* An intermittent obstructive jaundice.
* A fever.
* A gradual decline in general health.
The opacification of the biliary tree is used to specify the characteristics of this cholangitis, there are then:
- Strictures localized only to the extra hepatic bile duct, raises the differential diagnosis with post-traumatic stenosis.- Strictures localized only to intra hepatic or biliary dilatation, raises the differential diagnosis with congenital stenosis of the bile ducts within the liver.
The disease progresses to chronic retention that can lead to secondary biliary cirrhosis.Sclerosing cholangitis secondary to group together a large number of bile with very rare.
It is convenient to classify these patients into three groups: those whose ischemic origin is certain, those with ischemic possible; bile and other injuries.
The secondary biliary cirrhosis
Its starting point is the element responsible for initial obstructive cholangitis, plus the development of secondary sclerosing cholangitis, which causes a chronic progressive cholestasis.
According to "Scobie" and "Summerskill," the surgical wounds of the biliary tract are the main etiology in the case of repeated cholangitis preceding cirrhosis.The clinical picture is not specific, as the pathology, diagnosis is based primarily on the history and the discovery of obstruction.
But this favorable access without prejudice to the subsequent development, the appearance of recurrences may themselves give rise rapidly to serious complications, will indeed be based on the persistence or not of the obstacle and causal nature of the obstacle.
COMPLICATIONS
Early complications
Complications related to the onset of sepsis:
Gram-negative sepsis
Sepsis is characterized by significant and repeated shocks in the blood of pathogens from an outbreak of some kind.
Sepsis is likely to cause secondary outbreaks that will multiply more or less apparent.
Clinically it results:
* High fever which is the presence of bacteria in large numbers in the blood.
* Drop in blood pressure.
* Face greyish.
* Cold extremities.
* Tachycardia.
* Signs indicating a disorder of blood coagulation.
* Chills, asthenia.
* Malaysia, Splenomegaly.
* Difficulty breathing.
The diagnosis is confirmed by the laboratory through which a blood culture and determination of an effective antibiotic (for sensitivity) is made at the time of fever spikes. The appearance of multiple visceral involvement, has in some cases to confirm the clinical diagnosis.Finally, a septic shock endotoxin may be, with:
* Events kidney.
* Cardiovascular collapse.
* Hemorrhagic Syndrome.
* Centro lobular hepatic necrosis.
* Acute edematous pancreatitis or nérotico colitis.
The renal manifestations
Encompasses a range of syndrome of varying severity, ranging from simple functional renal failure in renal organic. These renal failure occur more readily in subjects with multiple defects, and those with a long history of bladder.
Clinically: it generally does not change the little picture of cholangitis:
* Jaundice, however, can change the type and take a look flamboyant.
* Hypotension is common.
Own signs of kidney disease (anorexia, nausea, vomiting, drowsiness, impaired consciousness), are difficult to distinguish from those of cholangitis.
In practice, it should be distinguished:
The benign forms: usually corresponding to functional renal failure with oliguria, urinary urea concentration is high, but creatinine is normal. They cause dehydration with hydro electrolytic disorders, but are reversible after fluid replacement and / or hydro electrolytic rebalancing.
Serious: with oligo anuria, diuresis or retained, but with azotemia and creatinine still high, and the significant decrease in urinary urea concentration.The cardiovascular collapse
Installation is quick and brutal, manifested clinically by:
- A fall in blood pressure.
- Tachycardia.
- A fast breathing.
- A fall in central venous pressure.
- Oliguria.
Sometimes profuse diarrhea and vomiting sometimes bleeding.
The hemorrhagic syndrome
With mucocutaneous bleeding, or hematemesis, or melena alone. GI bleeding in this case, is often related to stress peptic ulcers, the occurrence of disseminated intravenous coagulation aggravates the bleeding.
Loco regional complications
Extension of the inflammatory process and infection with various elements of the hepatic pedicle:Relatively frequent local complications (20% of cases), may pose difficult surgical problems, pédiculite this is seen especially in patients subjected to prolonged antibiotic therapy, for which the time of surgery was delayed.
Liver abscesses:Are the result of direct spread of infection, but may be the result of localization of metastatic sepsis.
Miliary abscesses:Are the most frequent single abscess is rarer, likely to surgical drainage.
Pédiculites and abscesses:Can cause internal fistula generally, and perforations in the peritoneum free or partitioned, they are difficult to diagnose.
Late Complications
Sclerosing cholangitis and secondary
They are usually defined as disorders of the biliary tract acquired, non-tumor, diffuse or multifocal. They are generally characterized by irregularities in caliber of the bile duct strictures and dilatations involving. The inflammatory and sclerosing character is more often inferred from the radiological appearance as shown by histological examination.
The secondary cholangitis should be distinguished from a primary sclerosing cholangitis, and other aspects of irregular bile ducts caused by a tumor, or a breach of the light of the bile ducts more than that of their wall.
Clinically it results:
* An intermittent obstructive jaundice.
* A fever.
* A gradual decline in general health.
The opacification of the biliary tree is used to specify the characteristics of this cholangitis, there are then:
- Strictures localized only to the extra hepatic bile duct, raises the differential diagnosis with post-traumatic stenosis.- Strictures localized only to intra hepatic or biliary dilatation, raises the differential diagnosis with congenital stenosis of the bile ducts within the liver.
The disease progresses to chronic retention that can lead to secondary biliary cirrhosis.Sclerosing cholangitis secondary to group together a large number of bile with very rare.
It is convenient to classify these patients into three groups: those whose ischemic origin is certain, those with ischemic possible; bile and other injuries.
The secondary biliary cirrhosis
Its starting point is the element responsible for initial obstructive cholangitis, plus the development of secondary sclerosing cholangitis, which causes a chronic progressive cholestasis.
According to "Scobie" and "Summerskill," the surgical wounds of the biliary tract are the main etiology in the case of repeated cholangitis preceding cirrhosis.The clinical picture is not specific, as the pathology, diagnosis is based primarily on the history and the discovery of obstruction.
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