Postoperative pain: a psychological assessment

Management of postoperative pain relieves suffering and leads to earlier mobilisation, a shortened hospital stay, reduced hospital costs, and increased patient satisfaction.


An effective postoperative management is not a standardised regime and is rather tailored to the needs of the individual patient.

Dr Sean Chetty, Deputy Head of the Department of Anaesthesiology and Critical Care at the Stellenbosch University, and an executive committee member of the Pain SA society, said that postoperative pain management should be individualised, personalised and focussed on the psychological state of the patient prior, during and after surgery.
Dr Milton Raff, past Chairman of the Pain Committee of the World Federation of Societies of Anaesthesiologists (WFSA)
but that attention needs to be given to pain management in developing countries.

“It has become evident that acute pain management must be the starting point for educational initiatives.
“Approximately 80% of all surgical patients experienced moderate to extreme pain following their surgery.
“Unrelieved pain has other consequences besides patient satisfaction. Adverse physiological and psychological effects may result from unrelieved severe acute pain. It can be concluded that there are physiological, psychological and economic reasons to ensure that patients receive effective acute pain therapy.”

Definition of pain

According to Anuj Gupta et al, postoperative pain is considered a form of acute pain due to surgical trauma with an inflammatory reaction and initiation of an afferent neuronal barrage. It is a combined constellation of several unpleasant sensory, emotional and mental experience precipitated by the surgical trauma and associated with autonomic, endocrine-metabolic, physiological and behavioural responses.

The impact of Perioperative Care

The practice of modern anesthesiology extends from preoperative period to the intraoperative period, and then into the postoperative period. Effective postoperative analgesia improves patients’ outcome as observed by a decrease in side effects, and reduced incidences of postoperative pain.
“Pain is a highly subjective experience, and no two patients will experience pain in exactly the same manner,” explains Chetty.
“Genetics, past experiences and emotional state will determine the manner in which a patient will experience pain, as well as the pain threshold of an individual. The perioperative period is therefore crucial in establishing
a patients specific intraoperative and postoperative pain management needs.”

The physiology of acute pain

Pain is a complex interaction of sensory, emotional and behavioral factors. There are no pain pathways, only nociceptive pathways. Nociception is modulated at the level of the spinal cord and interpreted by the cortex, resulting in varying degrees of discomfort and pain.

Acute pain is defined as pain of short and limited duration. The pain relates to an identifiable cause (trauma, surgery or inflammation). Acute and chronic pain represent a continuum of a process where inflammatory neuropathic visceral and somatic pain plays a role. The central nervous system (CNS) is not a hard-wired system. It allows for peripheral, central, intracellular and synaptic modifications. Acute pain can result in long- term changes and a subsequently modified response to sensory input (neuroplasticity).

“Essentially the primary role of managing pain in the postoperative period is to consistently monitor and manage the level of pain a patient will experience during the acute period which will typically last between 24 to 48 hours post-surgery. After major surgery, the management of postoperative pain can typically last a week, says Chetty.

Types of pain

Nociceptive Pain is the signal of tissue irritation, impending injury, or actual injury. Nociceptors in the affected area are activated and then transmit signals via the peripheral nerves and the spinal cord to the brain, activated
the complex spinal reflexes (withdrawal), followed by perception, cognitive and affective responses, and possibly voluntary action.

Nociceptive Pain is the result of the nervous system injury or malfunction, either in the peripheral or in the central nervous system. The pain may persist for months or years beyond the apparent healing of any damaged tissues. Neuropathic pain is frequently chronic.

Psychogenic Pain due to the psychological factors leading to an exaggerated or histrionic presentation of the pain problem.

Mixed Category Pain is caused by a complex mixture of nociceptive and neuropathic factors. An initial nervous system dysfunction or injury may trigger the neural release of inflammatory mediators and subsequent neurogenic inflammation.

Postoperative pain can be divided into acute pain and chronic pain. Acute pain is experienced immediately after surgery (up to seven days) and pain which lasts more than three months after the injury is considered to be chronic pain.

Adverse effects of pain

The aim of adequate pain management is to provide pain relief as a humane measure, as well as to minimise the multi-system deleterious effects caused by the stress response. A catabolic state, sympathetic stimulation and immuno-suppression are hallmarks of the stress response.

The endocrine system changes result in a catabolic state, increased adrenocorticotropic hormone, cortisol, antidiuretic hormone, cathecolamines, angiotensin II, interleukin (IL)-1 and IL-6, and tumour necrosis factor. Sympathetic stimulation results in an increased heart rate and blood pressure, increasing the risk of myocardial ischaemia. Pain limits coughing and decreases functional residual capacity, which, in turn increases the risk of atelectasis and pulmonary infection.

Decreased mobility results in an increased risk of deep vein thrombosis. Anxiety, helplessness, loss of control, an inability to interact and sleep deprivation all contribute to psychological disturbances, which can increase the risk of persistent pain developing.

Measurement and assessment of pain

According to Wells N, Pasero C and McCaffery M. pain assessment is recognised by virtually all of the pain guidelines as a crucial step in providing good pain management.

Verbal descriptor scale

The verbal descriptor scale (VDS) involves setting up five specific terms to describe pain; at the extremes are ‘no pain’ and ‘worst pain possible‘. In addition to those two poles, the patient may select ‘mild’, ‘moderate‘, or ‘severe’ pain.

Visual Analog Scale

The visual analog scale (VAS) involves a straight line of 10cm with tick marks, starting with 0 and indicating each centimeter; smaller lines may indicate millimeters. The patient is instructed that 0 indicates no pain and 10cm indicates the worst pain possible.

Numerical rating scale

The numerical rating scale works on a similar principle as the VAS, but instead of pinpointing the pain level on a straight line, the patient merely selects the number from 0 to 10.

Adjusting treatment according to the intensity of pain

The World Health Organisation recommends a treatment stepladder, based on the severity of the pain, available drugs and patient condition, to be utilised.

Pain Scale Interpretation Action
0/10 No pain No treatment
1- 3/10 Mild pain Simple analgesics: Paracetamol, NSAIDS
4- 7/10 Moderate Weak opioids: Tramadol, Codeine
8- 10/10 Severe Strong opioids: Morphine


Treatment Guideline

1.1 General information on Opiods:

Classification of Opiods

  • Opioid agonists
  • Opioid dualists: Both antagonism and agonism. (Theoretically, the side-effects should cancel one another out)
  • Opioid antagonists
  • Atypical opioids

Side-effects of Opiods

Respiratory depression, sedation, nausea and vomiting, pruritis, constipation and tolerance.

1.2. General information on Paracetamol

The following information is important with regard to paracetamol:

  • Very safe drug when used in appropriate doses
  • Caution should be exercised in patients with liver failure
  • An excessive dosage may cause irreversible liver failure
  • Use with caution or decrease the dose if there is: acute liver disease, alcohol- related liver disease, glucose-6-phosphate dehydrogenase deficiency.

1.3. General information on NSAIDS: Nonsteroidal Anti-Inflammatory Drugs (For mild to moderate pain relief)

Nonsteroidal anti-inflammatory drugs (nsaids) can be classified into:

  • Cyclo-oxygenase (COX-1 and 2) inhibitors J Selective COX-2 inhibitors
  • Specific COX-2 inhibitors.
  • Side-effects include the following:
  • Renal damage, especially if there is prior renal impairment or if the patient is hypovolaemic
  • Platelet impairment
  • Gastric erosions and haemorrhage
  • Possible poor wound healing (a concern of surgeons)
  • Asthma, which may be exacerbated in some patients.
  • Parenteral administration applies to the following:
    • Ketorolac
    • Lornoxicam
    • Parecoxib.

1.4. Approach to oral combination analgesics

A combination of the oral drugs are used extensively in South Africa. The rationale to combine drugs is to reduce the dose of each drug, therefore improving the side- effect profile. “However, it is important that practitioners are aware of the components in combination drugs,” says Chetty.

1.5 Local anaesthestics

Local anaesthetics are either short or long acting. Lignocaine is an example of a short-acting anaesthetic, and bupivacaine, ropivacaine and L-bupivacaine are examples of long-acting anaesthetics.
When administering a local anaesthetic, it is important to be aware of the following side-effects:

  • The effects of a toxic dose
  • Cardiotoxicity
  • Neurotoxicity.

According to the International Association for the Study of Pain (IASP), “Decades of research have established that acute pain after surgery has a distinct pathophysiology that reflects peripheral and central sensitisation as well as humoral factors contributing to pain at rest and during movement. This can impair functionality and often culminates in delayed recovery.”

Nociceptor activation, sensitisation, and hyperalgesia:

  • Surgical tissue trauma leads to nociceptor activation and sensitisation. As a result, individuals suffer ongoing pain at rest and increased responses to stimuli at the site of injury (primary hyperalgesia).
  • Different surgical procedures (including debridement for acute burn care) involve distinct organs and specific tissue within and adjacent to them, creating a variety of patterns of nociceptor sensitisation and differences in the quality, location, and intensity of postoperative pain.
  • Mediators released locally and systemically during and after surgery that contribute to nociceptor sensitisation include: prostaglandins, interleukins, cytokines and neurotrophins (e.g. nerve growth factor (NGF), glial-derived neurotrophic factor (GDNF), neurotrophin (NT)-3, NT-5, and brain-derived neurotrophic factor (BDNF)).
  • Decreased tissue pH and oxygen tension, and increased lactate concentration, persist at the surgical site for several days. These responses may contribute to peripheral sensitisation (e.g., muscle C-fibers) and spontaneous pain behaviour following an incision. Acid-sensing ion channels (e.g. ASIC3) likely transduce this ischemic-like signal.
  • Peripheral neutrophilic granulocytes (NGs) contribute to peripheral sensitisation and pain after surgical incision [3, 18]. Endogenous CD14+ monocyte responses (e.g., via the TLR4 signaling pathway) are associated with differences in the time course of postsurgical pain.
  • Nerves may be injured during surgery and hence discharge spontaneously. Spontaneous action potentials in damaged nerves may account for qualitative features of neuropathic pain that may be present early in the postoperative period and can evolve into chronic neuropathic pain.

Central sensitisation during acute postoperative pain:

  • Noxious input during and after surgery can enhance the responses of nociceptive neurons in the CNS (central sensitisation) thereby amplifying pain intensity.
  • The magnitude of central sensitisation depends on many factors, including the location ofthe operative site and the extent of the injury.
  • -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor mediated spinal sensitisation contributes to pain and hyperalgesia after incision.
  • Phosphorylation of the AMPA receptor GluR1 subunit at Serine-831 via protein kinase C gamma (PKC), but not other conventional PKC isoforms (PKC, I and II), leads to an increase trafficking of Ca2+ permeable AMPA receptors in theneuronal plasma membrane.
  • GluR1 is upregulated in the spinal cord ipsilateral to an incision via stargazin, a transmembrane AMPA receptor regulatory protein.
  • Other molecules involved in central sensitis ation after surgical incision involvephosphorylated extracellular signal-regulated kinases (ERK) 1/2, BDNF, Tumor necrosis factor) TNFa, iNOS, mitogen-activated protein kinase phosphatase (MKP)3, monoamine oxidase (MAO) B, toll-like receptor (TLR) 4 receptor and cyclooxygenase (COX) 2 (among others).
  • pinal inhibitory mechanisms may be able to prevent central sensitisation
    after surgery, for example via spinal -adrenoceptors, -Aminobutyric acid (GABA) receptors, or enhanced Glutamate transporters, among other mechanisms.
  • Opioids modulate central sensitisation in complex ways. Some in-vitro studies indicate that opioids can inhibit sensitisation of nociceptive pain pathways.
  • Clinical studies suggest that opioids actually amplify pain transmission one mechanism may be, for example, ketamine-sensitive phosphorylation of spinal NMDA receptors (NR2B at Tyr1472).

References available on request.

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