Assessing abdominal pain through history taking and physical examination

Transcription

1 Assessing abdominal pain through history taking and physical examination Abdominal pain can be a distressing experience for patients and presentations in primary or acute care pose diagnostic challenges to practitioners. In order to successfully manage a patient presenting with abdominal pain, it is imperative that the practitioner has a thorough, comprehensive understanding and knowledge of the methodological assessment of abdominal pain. In this article, Daniel Apau presents an brief overview of assessment for the types and origins of abdominal pain in practice. Daniel Apau is lecturer in public health and primary care, Department of Public Health, Primary Care and Food Policy, School of Community and Health Sciences, City University, London n Abdomen n Pain n History taking n Assessment n Examination Key words This article has been subject to double-blind peer review Pain threshold is determined by the nature of stimuli, the type of receptor involved, and the organization of pain pathways from the site of injury to the central nervous system. Psychosocial components such as ethnic and cultural background and the circumstances surrounding the nature of injury can modify patients perception of pain (Glasgow and Mulvihill, 2006). The abdominal cavity has complex sensory pathways making interpretation of the source of pain complicated for practitioners. Assessment of abdominal pain requires insight and understanding of pain conduction within the abdominal cavity. Sensory neuroreceptors in the abdominal cavity are localized within the mucosa and the thin layer of smooth muscle in the gastrointestinal tract as well as the peritoneum (Klish, 1983). Sensory transmitters that respond to noxious stimuli are involved in the regulation of secretions, motility and blood flow via local and central reflexes. Disordered regulation of these gastrointestinal functions such as bile secretion, peristalsis and blood flow can therefore induce pain (Glasgow and Mulvihill, 2006). The neuroreceptors involved in transmitting noxious stimuli in the abdominal cavity are type A delta fibres and type C delta fibres. Type A delta fibres terminate in the thalamus and therefore pain perceptions are perceived from direct location of pain. Type A delta fibres innervate cutaneous tissues and the parietal peritoneum and convey somatoparietal pain sensations which are sharp, sudden and well-localized, and usually follow acute injury or irritation from secretions such as pus, blood or bile (Doherty and Boey, 2003). Type C delta fibres terminate in the brain stem and accord poor pain perception. These are found in muscles, periosteum, mesentery, peritoneum and viscera and convey dull, burning, poorly localized and more gradual onset with longer duration pain (Senguta and Gebhart, 1994). The multisource nature of noxious stimuli in the abdominal cavity means practitioners face the difficult task of identifying the source and cause of pain. However, a good knowledge of patterns of pain transmission in the abdominal cavity would guide the practitioner in accurate chronological assessment to facilitate management of abdominal pain. Types of pain Visceral pain Visceral pain is experienced when noxious stimuli trigger visceral nociceptors. Pain is usually dull and poorly localized in the midline, epigastrium and periumbilical region or lower mid abdomen, as abdominal organs transmit nerve impulses to both sides of the spinal cord (Glasgow and Mulvihill, 2006). Visceral pain is described as cramping, burning, or gnawing with secondary autonomic effects such as sweating, restlessness, nausea, vomiting, perspiration and pallor. Visceral nociceptors are sensitive to stretching. Cutting, tearing or crushing of the viscera does not result in pain (Bonica and Graney, 2001). There are three types of visceral pain: 50 gastrointestinal nursing vol 8 no 7 September 2010

2 Tension pain colicky and cramping pain from forceful peristaltic contraction in an attempt to eject irritating substances, stretching of an organ due to distension from pus, bile or blood or as a result of partial or complete obstruction (Miller and Alpert, 2006), e.g. gastroenteritis, constipation and pancreatitis. The pain can subside with positional change and patients will usually shift positions to find the most comfortable during examination Inflammatory pain dull, deep and poorly localized and may be referred to other parts of the body initially due to innervation of type C fibres. If the cause of the condition is not checked, progression to severe, sharp localized pain will ensue with the involvement of parietal perineum through type A fibres Ischaemic pain sudden in onset, intense and progressive that does not respond well to analgesia (Doherty and Boey, 2003). Ischaemic pain usually involves infarction due to reduced or absent circulation. Somatoparietal and referred pain Somatoparietal pain arises from noxious stimulation of the parietal peritoneum and is generally more intense and precisely localized than visceral pain. Parietal pain is usually aggravated by movement or coughing. Referred pain is felt in areas far from the diseased organ and is due to visceral and somatic afferent neurones converging on second order neurones in the spinal segment (Glasgow and Mulvihill, 2006). Generally referred pain appears as the noxious visceral stimulus and becomes more intense, e.g. diaphragmatic irritation from subphrenic abscess or haematoma could produce shoulder tip pain (Glasgow and Mulvihill, 2006; Porter et al, 2008). Implications for practice Good knowledge and ability to distinguish between the various types of visceral pain will get the practitioner a step closer in determining the underlying pathology. When a patient describes the pain as deep, dull, vague or difficult to localize, then the noxious stimuli is likely to be caused by type C fibres, indicating the primary cause of pain is likely to be organ-based. On the other hand a sharp, localized, acute pain is likely to involve extension outside of the organ into the parietal peritoneum and might involve leakage of bile, blood or pus (Klish, 1983). A variety of tests might therefore be required to elicit a condition that initially exhibits referred pain and later somatoparietal pain, for example, in appendicitis where the pain is initially described as midabdomen, periumbilical and when the visceral peritoneum becomes inflamed, the pain becomes more localized. History taking The goal of evaluating the patient with abdominal pain is to establish an early, efficient and accurate diagnosis. Ascertaining chronological description of the onset, location, intensity, character, aggravating or alleviating factors, other symptoms, medical history, medication and social history will shed more light on the nature of the problem. All elements of history taking outlined in Table 1 should be discussed and carefully considered. Physical examination Physical examination should include inspection, auscultation, percussion, palpation and other special manoeuvres to aid diagnosis. Table 1. Factors to consider in ascertaining severity of the problem History Rapidity of onset and progression is a measure of the severity of underlying disorder Progression Progression of pain is an important factor as pain from disorders such as gastroenteritis are self-limiting and will ease off whereas pain from appendicitis will progress Location Changes in location of pain could indicate progression from visceral to parietal irritation which can be an indication of progressing severity of condition Intensity/ character Aggravating and alleviating factors Associated symptoms Past medical history Family/social history This is difficult to measure and the practitioner has to take into consideration ethnic and cultural interpretation of pain Pain characteristics in relation to positional changes is significant. Patients with somatoparietal irritation such as peritonitis are motionless due to pain whereas patients with visceral type of pain such as gastroenteritis, renal colic, pancreatitis find comfort in positional changes Symptoms such as fever, chills, weight loss, nausea, vomiting, flatulence, diarrhoea, constipation, jaundice and dysuria may give a clue as to the cause of abdominal complaint Important to elicit possible causes of pain such as adhesions as a result of previous abdominal surgery Information obtained will shed more light on possible cause of pain vol 8 no 7 September 2010 gastrointestinal nursing 51

3 Inspection Physical examination should commence with the patient s appearance, ability to engage in conversation, breathing pattern, posture in bed, degree of discomfort and facial expression. The abdomen should be observed for pulsations or peristaltic movements which could indicate abdominal aneurysm or intestinal obstruction respectively. The abdomen should be inspected for distension, previous abdominal surgical scars, ecchymosis and visible distension. Old surgical scars could give an indication of possible adhesions. Auscultation Auscultation the act of listening for sounds using a stethoscope should be done with the patient positioned comfortably in the supine position if possible. The health professional should auscultate all four abdominal quadrants in enough time to elicit the presence of bowel sounds, delineating exaggerated bowel sounds and hyperactive peristalsis. Exaggerated bowel sounds may indicate enteritis and hypoactive bowel might indicate the presence of paralytic ileus. The health professional should auscultate for bruits and friction rubs which could indicate abdominal aneurysm or splenic infarct. Percussion Percussion is required to determine if underlying tissues or organs are air-filled, fluid-filled or solid. This is undertaken by using the tip of the right middle finger (the plexor finger) to strike the distal interphalangeal joint of the pleximeter finger. Percussion is needed to determine the borders of organs. It can reveal peritoneal irritation and is useful for ascertaining the presence of free fluid or air. Any large areas of dullness may indicate the presence of abdominal mass. Figure 1. Psoas test to assess for irritation of the iliopsoas group of hip flexors in the abdomen from appendicitis or peritonitis. Palpation Light palpation enables assessment of local and generalized tenderness and peritoneal irritation. Deep palpation will elicit guarding or rebound tenderness, which could be an indication of peritoneal irritation. It is important to gauge tolerance, as patients with abdominal pain might not tolerate deep palpation. The health professional must be cautious of possible aggravation of rupture or perforation on deep palpation. Figure 2. Obturator sign test increased abdominal pain suggests irritation of the obturator muscle which could indicate appendicitis or peritoneal inflammation. Special manoeuvres The following special manoeuvres are required to assess specific conditions such as appendicitis, cholecystitis or general peritoneal irritation from possible appendicitis: Rovsing s sign deep palpation on the left lower quadrant of the abdomen elicits pain on the right lower quadrant. This is an indication of referred pain and therefore suggestive of peritoneal irritation Murphy s sign test performed by hooking four fingers underneath the costal margin in the right upper quadrant creating a downward pressure. As the patient takes a deep breath, the gall bladder descends to touch the examiner s fingers 52 gastrointestinal nursing vol 8 no 7 September 2010

4 producing pain and stopping inspiration this may indicate acute cholecystitis Costovertebral angle tenderness assessed on suspicion of pyelonephritis or renal calculi. The palm of one hand is placed on the costovertebral angle region and a fist used to strike the hand to generate vibrations in the kidneys to elicit tenderness Psoas sign to assess for irritation of the iliopsoas group of hip flexors in the abdomen from appendicitis or peritonitis. A hand is placed against the patient s right knee and the patient raises his/her thigh against the resistance of the hand. Alternatively the patient lies on the left side and extends the right leg at the hip (Figure 1). The anatomical basis for the psoas sign test is that relative proximity of the appendix to the psoas muscle causes more irritation and pain when these muscles are stretched (visceral pain more sensitive to stretching) Obturator sign test performed by raising the patient s right leg with the knee flexed and internally rotating at the hip (Figure 2). Increased abdominal pain suggests irritation of the obturator muscle which could indicate appendicitis or peritoneal inflammation. Laboratory assessment There are some laboratory, radiological and point of care investigations that may narrow down and provide clues to the causes of abdominal pain (Table 2). After a complete history and physical examination, imaging studies might not be necessary for all abdominal pain. Which type of abdominal imaging to use should be a decision based on the modalities available and the likelihood of producing the most accurate finding to help the management of the patient. Conclusions The primary goal of management is to identify emergencies and to transfer or resuscitate the patient as the condition requires. In the acute setting, the health professional should follow the ABCD resuscitation principles (airway, breathing, circulation, disability assessment) to maintain homeostasis while waiting for the required intervention. In the primary care setting immediate transfer may be required without delay, depending on the situation. n Table 2. Radiological, laboratory and point of care investigations into the causes of abdominal pain Test/investigation Full blood count Platelets Haemoglobin Amylase C-reactive protein Pregnancy test Urinalysis Electrocardiogram Computerized tomography scan Abdominal/pelvic ultrasound Plain abdominal X-ray Rationale Bonica J, Graney D (2001) General considerations of abdominal pain. In: Loeser J, Butler S, Chapman C, Turk D, eds. Bonica s Management of Pain. 3rd edn. Lippincott Williams and Wilkins, Philadelphia PA Doherty GM, Boey JH (2003) The acute abdomen. In: Way L, Doherty GM, eds. Current Surgical Diagnosis and Treatment. 11th edn. Lange, New York NY Glasgow RE, Mulvihill SJ (2006) Acute abdominal pain. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran s Gastrointestinal and Liver Disease. 8th edn. Saunders Elsevier, Philadelphia PA Klish WJ (1983) Visceral pain. In: Chey WY, ed. Functional Disorders of the Digestive Tract. Raven Press, New York NY Longmore M, Wilkinson I, Davidson E, Foulkes A, Mafi A (2010) Oxford Handbook of Clinical Medicine. 8th edn.oxford University Press, Oxford Miller SK, Alpert PT (2006) Assessment and differential diagnosis of abdominal pain. Nurse Pract 31(7): Porter TF, Branch DW, Scott JR (2008) Early pregnancy loss. In: Gibbs RS, Karlan BY, Haney AF, Nygaard I, eds. Danforth s Obstetrics and Gynecology. 10th edn. Lippincott Williams & Wilkins, Philadelphia PA Senguta JN, Gebhart GF (1994) Gastrointestinal afferent fibres and sensation. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract. Raven Press, New York NY Raised white blood cell count could indicate peritonitis Raised platelets could indicate inflammatory disease or chronic gastrointestinal blood loss Reduced haemoglobin is suggestive of gastrointestinal bleeding Raised amylase levels supports diagnosis of acute pancreatitis, cholecystitis, ectopic pregnancy, perforated peptic ulcer Acute phase protein is indicative of ongoing infection or inflammation Mandatory for all patients of child-bearing age with abdominal pain Mandatory in all abdominal pain presentation to exclude urinary tract infection or renal calculi To exclude myocardial infarction More sensitive, accurate and specific than a normal X-ray Easier to organize and can be done at the bedside. It can help identify renal stones, gallstones, appendicitis, free peritoneal fluid and gynaecological problems but might prove technically difficult in an obese patient Checks for dilated loops, faecal impaction or loading, calcification in gallstones and aortic aneurysm From: Glasgow and Mulvihill (2006); Longmore et al (2010) vol 8 no 7 September 2010 gastrointestinal nursing 53

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