




































American International Journal of Multidisciplinary Scientific Research 

Vol. 1, No. 2; 2018 

Published by Centre for Research on Islamic Banking & Finance and Business 

 

 

9 
 

Basics of Acute Postoperative Pain 
 

 

Alaa Ali M. Elzohry MD
1
 & Ali M. El Foli

2 

 

1
ICU and pain Relief, South Egypt Cancer Institute, Assiut University, Egypt 

2
Pharmacology Department, Faculty of Medicine, Al Azhar Assuit University, Egypt 

Correspondence: Alaa Ali M. Elzohry,MD., Department of Anesthesia, ICU and Pain Relief, South Egypt Cancer 

Institute, Assiut University, Arab Republic of Egypt. Phone: +20-88-2060010  ،01007356462.Email: 

alaa.zohiry@hotmail.com 

 

Received: August 1, 2018              Accepted: August 28, 2018             Online Published: September 8, 2018   

 

 

 

Abstract 

Acute pain is an important fear for most patients and influences their recovery and overall experience. Poorly 

treated, it could lead to undesirable effects and patient dissatisfaction. Hence, it is important to understand, assess 

and treat acute pain effectively. Pain management has been transferred from intraoperative into per operative period 

throughout the emergence of modern anesthesiology. Pain management in postoperative period is one of the most 

essential components of sufficient post-surgical patients care. The objective of this review is to define and 

demonstrate the risks and different sequelae of acute post operative pain. 

 

Keywords: General Anesthesia-Regional Anesthesia- Acute Post Operative Pain -Upper Abdominal Surgery. 

   

1. Introduction 

Ronald Melzack said that "By any reasonable code, freedom from pain should be a basic human right, limited only 

by our knowledge to achieve it". It is the basic duty of all healthcare professionals to relieve pain, and the most 

important indication for treating pain after surgery is humanitarian. [1]                                                                                                          

Acute pain is an important fear for most patients and influences their recovery and overall experience. Poorly 

treated, it could lead to undesirable effects and patient dissatisfaction. Hence, it is important to understand, assess 

and treat acute pain effectively. [2] 

Pain may be classified according to its presumed etiology; nociceptive pain is due to the stimulation of nociceptors 

by noxious stimuli and neuropathic pain is the result of dysfunction of the nervous system. Pain may also be 

classified into somatic and visceral pain. An alternative classification is based on duration. [3] 

Acute pain is defined as ‘pain of recent onset and probable limited duration. It usually has an identifiable temporal 

and causal relationship to injury or disease’. The point at which acute pain becomes chronic has been suggested at 

about 12 weeks or when the pain is no longer thought to be due to the initial insult. [4] 

Pain associated with any surgery can be divided into somatic pain and visceral pain. Therefore, when performing 

epidural analgesia for abdominal surgeries, both the abdominal wall innervations and the afferent visceral 

innervations, must be targeted to provide optimal analgesia. The  innervations  of  the  abdominal  wall  has  a  

segmental  dermatomal  distribution  and  is supplied by the anterior and lateral cutaneous branches of the ventral 

rami of the seventh to twelfth intercostal nerves (T7-12). [5] 

2. Pain Perception and Nociceptive Pathways 

The ability of the somatosensory system to detect noxious and potentially tissue-damaging stimuli is an important 

protective mechanism that involves multiple interacting peripheral and central mechanisms. The neural processes 

underlying the encoding and processing of noxious stimuli are defined as ‘nociception’. [6] In addition to these 

sensory effects, the perception and subjective experience of ’pain’ is multi factorial and will be influenced by 

psychological and environmental factors in every individual.  



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Acute pain perception begins with activation of specific sensory nerves, termed nociceptors. These are un-

encapsulated free nerve endings that are present in the skin, deep somatic tissue and viscera. Providing the stimulus 

is suitably intense, high threshold nociceptors will still activate in the absence of actual tissue damage. Nociceptors 

are probably activated by mechanical distortion of the nerve leading to an increase in H+ and K+ concentration. 

Nociceptors can be divided into two main classes; A-delta and C fibers. The main properties of these fibers are 

summarized in the table (1) below. [7]  

 

Table (1): Classification and properties of neurons. 

 Conduction Myelination Sensation Receptors 

A-delta 10-40 ms-1 Yes Sharp, immediate High &  

low threshold 

A- beta > 40 ms-1 Yes Light touch Low threshold 

C-fibers < 2 ms-1 No Dull, aching High threshold 

 

Multiple tracts and centers exist within the central nervous systems which are responsible for the transmission, 

modulation and perception of noxious stimuli. It is important to realize that these areas should not be considered as 

fixed or functioning in isolation. Rather, they are subject to change from both descending and ascending pathways 

and can alter or expand their connections to interact with adjacent nerves. [8] 

Cell bodies of afferent nerves lie in the DRG with fibers synapsing in the dorsal horn of the spinal cord. The output 

from the dorsal horn is however dependent on other neuronal input to the synapse. Afferent neurons may divide 

prior to entering the cord and send branches cephalic or caudal in the longitudinal tract of Lissauer before synapsing 

with dorsal horn neurons. The result of this being that a single C-fiber afferent may be responsible for innervating 

dorsal horn neurons at multiple spinal levels. [9] 

The gray matter of the spinal cord can be divided into ten physiologically and histological distinct layers known as 

rexed lamina. Laminae 1 to 6 and 10 are the sites that sensory nerves synapse with dorsal horn cells and are 

important in pain transmission. Laminas 7-9 are involved with motor function. [10] 

 
Figure (1): Spinal and Supra spinal pathways of Pain  



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3. Physiology of Pain 

The ability of the somatosensory system to detect noxious and potentially tissue-damaging stimuli is an important 

protective mechanism that involves multiple interacting peripheral and central mechanisms. The detection of 

noxious stimuli requires activation of peripheral sensory organs (nociceptors) and transduction into action potentials 

for conduction to the central nervous system. Nociceptors are stimulated by chemical, thermal or mechanical 

damage and trigger the nociceptive impulses. [11] 

Nociceptive primary afferents are widely distributed throughout the body (skin, muscle, joints, viscera, meninges) 

and comprise both lightly myelinated A-delta fibers (diameter 2-5 mm) and slow-conducting unmyelinated C-fibers 

(diameter <2 mm). These fibers enter the dorsal horn of the spinal cord and synapse at different sites (Aδ at laminae 

II and V, C at laminae II). The substantia gelatinosa (lamina II) integrates these inputs and second-order neurons 

form the ascending spinothalamic and spinoreticular pathways on the contralateral side, figure (2). [12] 

The larger AB fibres conducting “touch” and descending pathways stimulate inhibitory interneurons within the 

substantia gelatinosa and inhibit C fibre nociceptive inputs. This is the basis of the gate theory of pain. Pain may be 

modified by altering the neural pathway from its origin at the nociceptor to its interpretation within the central 

nervous system by various agents. Psychological factors that influence the experience of pain include the processes 

of attention, other cognitive processes (e.g. memory/learning, thought processing, beliefs and mood), behavioral 

responses, and interactions with the person’s environment. [13] 

 
Figure 2: Physiology of pain 

 

4. Assessment and Measurement of Acute Pain 

Pain should be assessed within a biopsychosocial model that recognizes that physiological, psychological and 

environmental factors influence the overall pain experience. The assessment of acute pain should include a thorough 

general medical history and physical examination, a specific ‘pain history’ and an evaluation of associated 

functional impairment along with any side effects of treatment. In acute pain management, assessment must be 

undertaken at appropriately frequent intervals. [14] 

Sometimes associated factors such as hyperalgesia, the stress response (e.g. plasma cortisol concentrations), 

behavioral responses (e.g. facial expression), functional impairment (e.g. coughing, ambulation) or physiological 

responses (e.g. changes in heart rate) may provide additional information. [15] 

The assessment of acute pain should include a thorough general medical history and physical examination, a specific 

‘pain history’ and an evaluation of associated functional impairment. In acute pain management, assessment must be 

undertaken at appropriately frequent intervals. At these times, evaluation of pain intensity, functional impact, and 

side effects of treatment must be undertaken and recorded using tools and scales that are consistent, valid and 

reliable. [16] 



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The well-known visual analogue scale (VAS) and numeric rating scale (NRS) for assessment of pain intensity agree 

well and are equally sensitive in assessing acute pain after surgery, and they are both superior to a four-point verbal 

categorical rating scale (VRS). They may be used for worst, least, or average pain over the last 24 h, or during the 

last week. [17] 

Assessment of pain immediately after surgery can be more difficult and lead to greater inter patient variability in 

pain scores because of transient anesthetic-related cognitive impairment and decreases in visual acuity. (Machata et 

al, 2009 ). 

 
 

Figure 3: Commonly used one-dimensional pain intensity scales: the 11-point NRS, the VAS from no pain [0] to 

worst pain imaginable [10] and the four-point categorical verbal rating scale (VRS)  

5. Adverse Physiological and Psychological Aspects of Pain 

Clinically significant injury such as surgeries responses can lead to a range of physiological effects which may lead 

to adverse clinical effects. Patients at greatest risk of adverse outcomes from unrelieved acute pain include very 

young or elderly patients, those with concurrent medical illnesses and those undergoing major surgery. [18] 

Sustained acute nociceptive input, as occurs after surgery can also have a major influence on psychological function, 

which may in turn alter pain perception. Failure to relieve acute pain may result in increasing anxiety, inability to 

sleep, demoralization, a feeling of helplessness, loss of control, inability to think and interact with others -in the 

most extreme situations, where patients can no longer communicate, effectively they have lost their autonomy. [19]  

Aggressive perioperative pain prevention can yield both short-term and long-term benefits as unrelieved pain affects 

patient recovery, prolongs hospital stays, increases hospital morbidity, and adds to the burden of growing health-

care costs. In total, there are many important reasons for aggressive acute pain management. [20]   

Postoperative pain is considered a form of acute pain secondary to surgical trauma and is associated with an 

inflammatory reaction and subsequent pathway of afferent neuronal signals. Acute postoperative pain is associated 

with autonomic, endocrine-metabolic, physiological, and behavioral responses summarized in following table (2) 

[21]  

 

Table 2: Effects of surgery, including local and systemic inflammatory responses and mediated responses  

    Local and systemic inflammatory responses Mediated responses 

   Increase in proinflammatory cytokines, 

e.g., IL-1, IL-6, TNF 

 

     Decrease in anti-inflammatory cytokines 

 

Changes in acute phase protein 

 

Changes in coagulation/fibrinolysis 

 

Decrease in other cascade systems 

 

Increase in catabolic hormones, e.g., 

cortisol, catecholamines, glucagon 

 

 

Decrease in anabolic hormones, e.g. 

insulin and testosterone 

 

Increase in pain 

 

Increase in autonomic reflexes 

 

Decrease in afferent neural barrage 

 

 

 



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Table 3: Adverse effects of undertreated acute pain  

Cardiovascular Tachycardia, hypertension, increased peripheral vascular resistance, 

increased myocardial oxygen consumption, myocardial ischemia 

and/or infarction, altered regional blood flow, deep vein thrombosis, 

pulmonary embolism. 

Respiratory Reduced lung volumes, atelectasis, decreased cough, sputum retention, 

infection, hypoxemia. 

Gastrointestinal Decreased gastric and bowel motility, constipation, increased risk of 

bacterial transgression of bowel wall. 

Genitourinary Urinary retention 

Neuroendocrine/ 

metabolic 
 -Increased catabolic hormones: glucagon, growth hormone, vasopressin, 

aldosterone, renin and angiotensine. 

-Reduced anabolic hormones: insulin, testosterone 

-Catabolic state leading to hyperglycemia, increased protein breakdown 

negative nitrogen balance leading to impaired wound healing and muscle 

wasting. 

Musculoskeletal Muscle spasm, immobility with increased risk of deep vein thrombosis, 

muscle wasting leading to prolonged recovery of function. 

Psychological Anxiety, fear, helplessness, sleeps deprivation, leading to increased pain. 

Central nervous Chronic pain state related to central sensitization. 

 

Acute surgical pain causes a global sympathetic response capable of increasing heart rate, peripheral vascular 

resistance, blood pressure, and subsequently cardiac output. This sympathetic cascade can increase the oxygen 

demand of the myocardium and potentiate myocardial ischemia, especially in patients with preexisting coronary 

artery disease. [22]   

Acute pain has also been found to decrease limb blood flow by directing blood away from skin and viscera and 

toward vital organs. This decrease in extremity blood flow may impair wound healing and increase muscle spasm. 

Postoperative pain may also reduce patient mobility, promoting venous stasis. Increases in fibrinogen and platelet 

activation related to surgical trauma will increase blood coagulability. These factors together increase the risk of 

venous thromboembolism. [23]  

Data suggest that "the use of epidural anesthesia in the perioperative period results in less platelet activation and 

significantly better fibrinolytic function" thereby resulting in significant protection against Thromboembolic 

complications. This protection also may be related to the systemic effect of local anesthetics, which have been 

shown to have an antithrombotic effect. [24]  

Perioperative cardiovascular adverse events may result in considerably prolonged postoperative stay. Cardiovascular 

events warranting unanticipated hospital admissions are infrequent. Cardiovascular events occur with higher 

frequency among patients with preexisting cardiovascular diseases (e. g. hypertension, congestive heart failure). 

Increasing age is also associated with higher incidence of cardiovascular conditions among elderly patients. [25]  

6. Pain Management 

6.1 Non-pharmacological methods of pain relief 

 Preoperative explanation and education 

 Relaxation therapy 

 Hypnosis 

 Cold or heat 

 Splinting of wounds  

 Transcutaneous electrical nerve stimulation (TENS). 

6.2 Pharmacological and interventional methods of pain relief 

There are many techniques available for management of postoperative pain including: 

 Intravenous administration of opioids and non-steroidal anti-inflammatory drugs, alpha-adrenergic drugs; 

 Infiltration of local anesthetics; 

 Nerve blocks; 

 Epidural techniques; 

 Intratechal technique. [26]  

All of these techniques have benefits and risks (advantage and disadvantage) Patient control analgesia (PCA) is one 

of the most common techniques for postoperative pain management. This device is under patient control 



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intermittently or continuously, and infuses IV opioids or non- opioids. The use of intravenous opiates is still limited 

because of side effects such as respiratory depression. [27]  

Pre-emptive Analgesia: 

The administration of analgesia before surgery (preemptively) may be effective in reducing the postoperative pain 

from surgery by preventing the peripheral and central sensitization caused initially by surgical incision and later by 

inflammatory injury. There are studies that support the effectiveness of preemptive analgesia. However, other 

studies concluded that there was a lack of evidence for preemptive treatment with NSAlD's, intravenous opioids, and 

ketamine, peripheral local anesthetics, and caudal analgesia. [28]  

The effectiveness of preemptive analgesia is likely to remain a controversial issue for some time. Despite this, the 

preoperative administration of non opioid analgesia, such as NSAlDs, ketamine, and local anesthetics, prior to 

surgical incision is an important component in reducing postoperative pain scores and analgesic requirements in the 

first 24 hours after discharge. [29]  

Regional anesthesia and analgesia can be used to significantly reduce postoperative pain scores and spare the use of 

systemic opioids. Regional anesthesia can be performed at the neuraxis (epidural and intrathecal), the nerve root 

(paravertebral), and the peripheral nerve (transversus abdominis plane) level. Local anesthetic deposition at these 

sites will selectively block nerve conduction and result in different analgesic and side effect profiles. [30]  

7. Conclusion  

Acute postoperative pain is multifactorial with complicated Pathophysiology, but careful history and good 

assessment lead to ideal selection of treatment plane either medications or interventions according to operation 

performed. Interventional methods are favorable due to many reasons; avoiding chronic pain and decreased side 

effects of systematic medications as opioids. 

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