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Monday, 14 May 2012

abdominal colic diagnostic and management

Colicky abdominal

INTRODUCTION

Before discussing the pain of colic, will be presented in advance of abdominal pain in general. Abdominal pain resulting from the three channels, namely (Mahadevan, 2005):

• Abdominal viscera
Usually caused by distension of hollow organs or the tension in the capsule of solid organs. A rare cause of ischemia when the network is experiencing congestion atau inflamasi to sensitasion end visceral nerve pain and lower pain threshold. Pain inisering an early manifestation of a disease or discomfort a sense vague until the colic. If the organ is engage affected by peristaltic movements, the pain is often intermittent described as, cramps or colic.

• In this pain, bilateral pain due to nerve fibers, not myelin and entering spinal cord at varying levels, the viscera and abdominal pain is usually felt dull, hard to be localized and felt the middle body. Pain comes from the region of the abdominal viscera are referring origin of the embryonic organ. Foregut structures such as the stomach, duodenum, liver, biliary tract and pancreas produce upper abdominal pain, often perceived as pain epigastric region. Midgut structures such as the jejunum, ileum, appendix, and ascending colon causing pain periumbilikus. While the structure of the hindgut as the transverse colon, genitourinary system kolon desendens and cause lower abdominal pain.


• Abdominal pain parietal (somatic)
Parietal or somatic abdominal pain resulting from ischemia, inflamasiatau tension of the parietal peritoneum. Afferent nerve fibers that transmit pain stimulus bermielinisasi to the dorsal root ganglion and at the same dermatomal of origin of the pain. For this reason Yeri parietal  this is in contrast with visceral pain, can often be painful stimuluslocalized to the homelands. Is perceived to be a sharp pain, like a knife wound and survive; coughing and movement can trigger pain it. These conditions resulted in signs of physical examination can be searched delicate flavor, guarding, rebound pain and stiffness padaabdomen are palpable. Clinical presentation of appendicitis can of pain visceral and somatic. Pain in early appendicitis pain often in the form of periumbilikus (viscera), but localized in the region of the right quadrant bawahketika inflammation spreads to the peritoneum (parietal).

• Referred pain
Referred pain is pain that is felt at a distance from the diseased organ. This pain is produced from neuronal pathways afferent central terbagiyang from different locations. Examples are patients with pneumonia may experience abdominal pain due to neuron T9 distribution divided by the lungs and abdomen. Another example is the epigastric pain associated with myocardial infarction, pain in the shoulder associated with irritation of the diaphragm (eg, splenic rupture), nyeriinfrascapular pool associated with the disease and testicular pain associated with urethral obstruction.


Colicky abdominal pain

DEFINITION

Colicky abdominal pain is a pain in the form of intermittent severe attacks that can be localized and felt like a sharp feeling. The mechanism of this pain is due to either partial or total obstruction of hollow organs which contain smooth muscle tissue or organ involved is influenced peristalsis.
Classification of colicky abdominal
Classification based on etiology of some of them:



A. Mechanical
o Adhesion / postoperative adhesions (90% of mechanical obstruction)
o Carcinoma
o Volvulus
o Intussusception
o obstipasi • Polyps
o Stricture
2. Functional (non mechanical)
paralytic ileus o
o spinal cord lesions
o regional enteritis
o Electrolyte imbalance
o Uremia

Classification based on the location of the diantanya biliary colic, renal colic and colic due to intestinal obstruction (Gilroy, 2009).

A. Biliary colic

Biliary colic is a symptom of discomfort felt by patients dansering not accompanied by other clinical signs. This pain is gejalaklinis of gallstone disease (kolelitiasis / koledokolitiasis). Because pain is a symptom, then some other diseases also can give the same symptoms. Figure 1.1 shows the blockage of bile (Gilroy, 2009).







Figure 1.1 gallstone blockage that causes pain of biliary colic (Gilroy, 2009).

Biliary colic pain is not perceived accurately as colic. This term implies a paroxysmal pain up and down, and umumnyakonstan and increased slowly progressive. This felt for a moment pain after eating (Gilroy, 2009).
Visceral pain originating from the collision of gallstones in cystic duct ampulla of Vater danatau. The results of the collision was caused distension and kandungempedu or biliary tract and this distension activates afferent neuronsensori. Pain inflicted can not be localized and generally feel well in the middle to dermatomes T8 / 9 (middle epigastrium, kuadaran top right).Generally localized pain showed complications or koledokolitiasis yaitumisalnya kolelitiasis cholecystitis, cholangitis, pancreatitis. Some locations yangmungkin stone blockage can be seen in Figure 1.2 (Gilroy, 2009).




Figure 1.2 Location of possible blockage (Gilroy, 2009)
anamnesis

Biliary colic usually comes on suddenly and reach the intensity maksimumdalam 60 minutes at two-thirds of the patients. The pain usually goes without fluctuations and disappear gradually over 2-6 hours. Pain lasting longer than 6 hours should be suspected acute as kolesistitis (Gilroy, 2009).

physical examination

Initial examination often reveals an individual's sweaty, pale, and discomfort. Vomiting may accompany a sense of sakit.Pemeriksaan can reveal some physical featuresassociated with gallstone formation (eg, overweight, middle-aged, female). Patients with biliary colicwithout complications not have a fever, chills, hypotension, or other signs of a significant systemic process. Sinustachycardia is common during illness. Reflective pain, prisoners, no bowel sounds, or a palpable mass supports an alternative diagnosis (Gilroy, 2009). Figure 1.3 shows the location of biliary pain in the abdominal region (Platt, 2008).

Figure 1.3 Location of biliary colic pain (Platt, 2008).

Management

Treatment given depends on the symptoms experienced by patients. If the pain can be very powerful pain reliever that is golongannarkotik meperidine (pethidine) at a dose of 1 to 1.5 mg / kg IM every3 hours. If vomiting can be given metoclopramide. Nothing can guarantee the operation satupunintervensi as biliary colic complications that can not subside with conservative treatment (Gilroy, 2009).

2. Renal colic

This type of pain known as colic renal colic biasanyadimulai in mid-upper back of the lateral costovertebral angle and sometimes subkosta. Then spread to the inferior and anterior to the groin. The pain produced by colic ginjalt mainly due to the widening, stretching, and seizures caused by acute urinary tract obstruction. When developing chronic obstructive beratnamun, as in some types of cancer, usually painless (Leslie, 2010).

Colic is a misnomer because renal colic pain tends tetapkonstan, whereas intestinal or biliary colic usually somewhat intermittent and often lost to come. The pattern of pain depends on the individual pain threshold and perception and the speed and degree of changes in hydrostatic pressure in the proximal ureter and renal pelvis. Urinary tract peristalsis, stone migration, and on his side or play rock dapatmenyebabkan exacerbation or extension of ginjal.Tingkat colicky pain severity depending on the degree and location of obstruction, rather than on the size of the stone. A patient can often lead to the location of the maximum sickest, are likely to be the site of obstruction salurankemih (Leslie, 2010).

Phase of acute attacks of renal colic

Real pain attacks tend to occur in bertahapdapat predicted, with the pain reached its peak in most patients within 2 hours. Pain roughly follow dermatomT-10 to S-4. The entire process usually lasts 3-18 hours. Renal colic can be described dalam3 clinical phase (Leslie, 2010).

a) The acute phase
Typical attack began in the morning or at night, waking the patient from sleep. When starting the day, pasienyang often describe the attacks as slowly dandiam secretly. The level of pain may increase to intensitasmaksimum just 30 minutes after the initial onset or lebihlambat. Patients feel the pain reaches a maximum 1-2 jamsetelah commencement of renal colic attack.

b) Phase constant
Once the pain reaches maximum intensity, are likely to be treated or reduced tetapkonstan spontaneously. This phase usually lasts 1-4 hours but can last longer than 12 hours in some cases. Most of the patients arrived at UGDselama phase of the attack.

c) Phase subside
During the final stages, pain decreased quite rapidly, and the patient finally was relieved. This phase can occur spontaneously at any time after the initial onset of colic. The patient may fall asleep, especially if they have been given a powerful analgesic drug.

Kidney pain nerve fibers mainly in the form of preganglionic sympathetic nerves that reach the level of spinal cord T-11 to L-2 through the dorsal nerve roots. Aortorenal, celiac and inferior mesenteric ganglia jugaterlibat. In the lower ureter, pain signals are also routed through the genitofemoral and ilioinguinal nerves. Erigentes nerve, which menginervasi intramural ureter and bladder, are responsible for some symptoms of the bladder. Figure 1.4 shows the distribution dan1.5 innervation in the kidney and urethral pain and pain Lokas renal / ureter in the abdominal region (Leslie, 2010)
.

Figure 1.4. Shows a picture of innervation on renal colic pain (Leslie, 2010)



Figure 1.5 shows the distribution of renal and urethral pain and Lokas renal / ureter in the abdominal region (Leslie, 2010)

• Ureter 1/3 proximal and renal pelvis: urinary tract stones from the pain tends to radiate to the pelvis and lumbar regions. On the right, this can be confusing with cholecystitis ataucholelithiasis, on the left, differential diagnosis includes pankreatitisakut, gastric ulcer disease, and gastritis (Leslie, 2010).

• Ureter 1/3 medial: Midureteral cause pain that radiates anterior and caudal. This pain can be easily midureteral specifically mimic appendicitis on the right or left side of acute diverticulitis (Leslie, 2010).

• Distal ureter: Distal ureteral stones cause pain radiating to the groin yangcenderung or testes in men or labia majora in women because the pain is referred from the ilioinguinal or genitofemoral nerve. If the stone is lodged in the intramural ureter, symptoms can appear similar to cystitis or urethritis. It includes symptoms of suprapubic pain, urinary frequency, urgency, dysuria, stranguria, pain at the tip of the penis, and sometimes intestinal symptoms such as diarrhea and tenesmus. These symptoms can be confused with pelvic inflammatory disease, ruptured ovarian cyst or torsion and menstrual pain in women (Leslie, 2010).

Nausea and vomiting often associated with acute renal colic and there disetidaknya 50% of patients. Nausea caused by neural pathways umumdari renal pelvis, stomach, and intestines and nerves through the celiac axis aferenvagal. This is often compounded by the effects of narcotic analgesics, which often lead to nausea and vomiting through direct effects on the motility GIdan through indirect effects on the chemoreceptor trigger zone dimedula oblongata. Nonsteroidal anti-inflammatory drug (NSAID) commonly can cause gastric irritation and GI (Leslie, 2010).

Nerve blocks have been successfully used both in diagnosis and treatment of colic kidneys, although they are more helpful in cases of acute cases kronisdaripada. Intercostal nerve blocks can be used to distinguish pain from chondritis, neuromas, and radiculitis of the actual sakitginjal. This is achieved by injecting agenanestesi, such as lidocaine, around the proximal nerve interkostaliske 11 or 12 at the location of pain patients experience pain. If injection causesrelieve your pain, the etiology of musculoskeletal peripheral nerves can be enforced (Leslie, 2010).
  
Microscopic examination of urine is an important part of the evaluation of suspected colicpatients with kidney disease. macroscopic hematuria or microscopic examination around 85% of cases. Lack of renal colic, microscopic hematuria is not Eliminate as a potential diagnosis. Attention should be given to the presence or absence of leukocytes, crystals, and bakteridan urine pH. In general, if the number of leukocytes in urine greater than 10 cells per high power field or greater than the number of cells red blood cells, suspected urinary tract infection (UTI) can ditegakkan.Menentukan urine pH also helps because, (1) with a pH over 6 lower than , 0, uric acid stones should be considered, and (2) with pH 8.0 lebihdari, infection with urea splitting organisms such as Proteus, Pseudomonas, or Klebsiella may exist. Urine crystals from kalsiumoksalat, uric acid, or cystine can sometimes be found in urinalisis. If da, this crystal is very good instructions for each type of rock underlying  (Leslie, 2010).

Management

Treatment early in the emergency room began with   gain acses vein to facilitate administration of fluids, analgesic and antiemetic medication. Many of the patients who experienced nausea and vomiting dehidrasikarena (Leslie, 2010). Doing provide hydration and diuretic therapy is a controversial pembantumasih. Some argue it can help spending a stone, but no one thought would add tekananhidrostatik thus increasing pain. However, the extra fluid harusdiberikan if patients with clinical or laboratory evidence of mengalamidehidrasi, diabetes or kidney failure (Leslie, 2010).
Protocols that are based on the possibility of spontaneous stone passage failure either because of urethral stricture, muscle spasm, local edema, inflammation and infection. Regimens are provided in the form (Leslie, 2010):
• ketorolac 10 mg oralsetiap 6 hours for 5 days.
• Nifedipine 30 mg per day PO for 7 days.
• Prednisone 20 mg PO 2 times a day for 5 days.
• Trimethoprim / sulfamethoxazole once daily for 7 days.
• Acetaminophen 2 tablets 4 times daily for 7 days.
• Prochlorperazine suppositories for nausea control.

The stone is stuck in the Calix can block the flow of Calix yangmenyebabkan tract obstruction and pain. Treatment with ESWL can be reasonable for the situation that the stone is suspected of causing symptoms dannyeri Calix (Leslie, 2010).

3. Colic due to intestinal obstruction

A small bowel obstruction (SBO) is caused by various pathological processes. The main cause of SBO in developed countries is postoperative adhesions (60%) followed by malignancy, Crohn's disease, and hernias, although some studies have reported Crohn's disease as an etiologic factor greater than neoplasia. One study from Canada melaporkanfrekuensi higher than SBO after colorectal surgery, gynecology diikutioleh surgery, hernia repair and appendectomies (Nobie, 2009). SBO can be partial or complete, simple (ie, nonstrangulasi) ataustrangulasi. Strangulation obstruction is a surgical emergency. If not diagnosed and treated properly, causing intestinal ischemia and morbiditaslebih and death (Nobie, 2009).

Obstruction of the proximal small intestine causes the dilatation of the bowel due to the accumulation of GI secretions and swallowed air. This bowel dilatation merangsangaktivitas secretory cells produce more fluid accumulation. It  cause increased  peristalsis both above and low obtructionksi with frequent watery stools and flatus early in its course (Nobie, 2009).

Vomiting occurs when the obstruction is proximal. Increased distention of the small intestine causing increased intraluminal pressure. This can cause compression of the intestinal mucosa leading to lymphatic kelymphedema wall. With higher intraluminal hydrostatic pressure, increase in capillary hydrostatic pressure of the liquid sehinggaketiga, electrolyte, and protein out into the lumen usus. loses fluid and dehydration can be severe and contribution to increased morbidity and mortality. Menyebabkaniskemia intestinal artery occlusion and necrosis. If untreated, it developed into a perforation, peritonitis, and death (Nobie, 2009). Picture 1.6  obstruksi intestinal pain location on the abdominal region.
Figure 1.6 Location of pain in the abdomen ostruksi intestine (Platt, 2008)

The clinical manifestations

Obstruction has a characteristic form or complete pasial ,simple or strangulation.
Manifestations may include (Nobie, 2009):

• Abdominal pain (characteristic in most patients)
• Pain, often described as cramping and intermittent, which lebihmenonjol in simple obstruction.
• Often, the clinical appearance may provide clues to estimate the location and nature of the obstruction. Pain lasted for several days, which became progressively and with abdominal distension, may be typical for obstruksiyang more distal.
• Changes in the character of pain may indicate a more serious komplikasiyang development (eg, constant pain or ischemic bowel strangulation).
• Nausea
• Vomiting, which is more associated with proximal obstruction
• Diarrhea (preliminary findings)
• Constipation (a late finding) as evidenced by the absence of bowel movement or pass gas.
• Fever and tachycardia, occur later and may be associated with strangulasi.
• History of abdominal or pelvic surgery before
• History of malignancy (particularly ovarian and colon)

Physical examination

Some things that are found from the physical examination include (Nobie, 2009):
• Abdominal distention
• hyperactive bowel sound occurs at the beginning of an effort to mengatasiobstruksi GI.
• The sound is decreased bowel occurs later
• exclude inkarserata hernia of the groin, the femoral triangle, and the obturator foramen.
• The findings on rectal examination toucher:
o Blood or faintly visible, indicating strangulasilanjutan or malignancy
o Mass, which shows the obturator hernia
• Check the common symptoms believed to be more diagnostic for bowel ischemia, namely:
Fever (temperature> 100 ° F)
o Tachycardia (> 100 beats / min)
o Signs of peritoneal

Cause

Some of the things that cause, among others (Nobie, 2009):
• The most common cause of SBO is postsurgical adhesions.
• Adhesion can be a cause of postoperative acute obstruction  on  4 weeks of surgery or chronic obstruction decades later.
• SBO incident parallel to the increase in the number of laparotomies performed in developing countries.
• The second most identified cause of SBO is common hernia inkarserata.
• Other etiologies of SBO including malignant tumors (20%), hernia (10%), inflammatory bowel disease (5%), volvulus (3%), and varied (2%).
• The cause of SBO in pediatric patients include congenital atresia, pyloric stenosis, and intussusception
Figure 1.7. Images showing some of the causes obstruksiusus fine (Kumar, 2008).

Management

Treatment early in the emergency room secaraagresif include fluid resuscitation, bowel decompression, providing analgesic and antiemeticdengan clinical indications, antibiotics and early surgery consultation. Decompression performed by placing a suction hose to the NGT to do isis GI and to prevent aspiration. Do not forget to always monitor the airway, breathing and circulation (Nobie, 2009).

CLINICAL colicky abdominal

A. Simple mechanics - the small intestine
Colicky (cramp) in the mid to upper abdomen, distension, vomiting bile early, increased bowel sounds (high pitched tinkling sounds at short intervals), minimal diffuse tenderness.
2. Simple mechanics - the small intestine
Colicky (cramp) midabdomen significant, severe distension, vomiting - little or nothing - and then have the dregs, bowel sounds and the sound of "hush" increase, minimal diffuse tenderness.
3. Simple mechanics - colon
Cramps (middle to lower abdomen), which emerged last distension, and vomiting (fekulen), increased bowel sounds, diffuse tenderness at a minimum.
4. Partial mechanical obstruction
Can occur with granulomatous bowel in Crohn's disease. Symptoms are cramping abdominal pain, mild distension and diarrhea.
5. Disturbance
Symptoms develop rapidly; severe pain, continuous and localized; distension are: persistent vomiting, usually decreased bowel sounds great nd localized tenderness. Stool or vomiting becomes dark or bloody or blood-containing vague.

EXAMINATION
o tension, pulse, respiration, temperature
o Examination of the abdomen: the location of pain, is there any tenderness / pain off
o Is there a liver enlargement, whether palpable mass
o Rectal examination: pain location at what time, is there any faeces, is there any blood
o Laboratory: Leukocytes and Hb



Examination support
• Abdominal x-ray showed gas or liquid in the intestines
• Barium enema showed a terdistensi colon, sigmoid folds filled with air or enclosed.
• Decreased levels of serum sodium, potassium and chloride from vomiting; WBC count increased with necrosis, strangulation or peritonitis and elevated levels of serum amylase because irritation of the pancreas by the folds of the intestine.
• Arterial blood gases may indicate metabolic acidosis or alkalosis.

Reference
  1. Gilroy, RK. 2009. Biliary colic, in E-Medicine. http://emedicine.com.
  2. Kumar, Abbas, Fausto.2008. Robbin’s and Cotran Pathologic Basis of Disease.
  3. Leslie, SW. 2010.. Nephrolithiasis, Acute Renal Colic, in E-Medicine.  http://emedicine.com
  4. Mahadevan, SV. 2005. An  introduction to Clinical Emergency Medicine. Cambridge University Press.
  5. Nobie, BA. 2009. Small Bowel Obstruction, in E-Medicine. http://emedicine.com
  6. Platt, M. 2008. Abdominal Pain in Current Diagnosis & Treatment Emergenvy Medicine. 6th edition. Mc. Graw Hill.

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