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Pharmacology
Assessment and Treatment of Pain in Adult Intensive Care Unit Patients
Jun Mo Park, Ji Hyun Kim
Korean J Crit Care Med. 2014;29(3):147-159.   Published online August 31, 2014
DOI: https://doi.org/10.4266/kjccm.2014.29.3.147
  • 17,978 View
  • 693 Download
  • 3 Crossref
AbstractAbstract PDF
In most cases, patients admitted to an intensive care unit (ICU) have suffered from severe trauma, undergone major surgery or been treated for a serious medical illness. Although they often experience more intense pain than general ward patients, they are frequently unable to communicate their experiences to health care providers, thus preventing accurate assessment and treatment of their pain. If appropriate measures are not taken to treat pain in critically ill patients, stress response or sympathetic overstimulation can lead to complications. The short-term consequences of untreated pain include higher energy expenditure and immunomodulation. Longer-term, untreated pain increases the risk of post-traumatic stress disorder. Because pain is quite subjective, the accurate assessment of pain is very difficult in the patients with impaired communication ability. The current most valid and reliable behavioral pain scales used to assess pain in adult ICU patients are the Behavioral Pain Scale and the Critical-Care Pain Observation Tool. Once pain has been accurately assessed using these methods, various pharmacologic and non-pharmacologic therapies should be performed by the multidisciplinary care team. Accurate assessment and proper treatment of pain in adult ICU patients will improve patients outcome, which reduces the stress response and decreases the risk of post-traumatic stress disorder.

Citations

Citations to this article as recorded by  
  • Nurses’ knowledge, practice, and associated factors of pain assessment in critically ill adult patients at public hospitals, Addis Ababa, Ethiopia
    Temesgen Ayenew, Berhanu Melaku, Mihretie Gedfew, Haile Amha, Keralem Anteneh Bishaw
    International Journal of Africa Nursing Sciences.2021; 15: 100361.     CrossRef
  • Impact of Pain Management Algorithm on Pain Intensity of Patients with Loss of Consciousness Hospitalized in Intensive Care Unit: A Clinical Trial
    Zahra Dehghani, Asadollah Keikhaei, Fariba Yaghoubinia, Aliakbar Keykha, Masoom Khoshfetrat
    Medical - Surgical Nursing Journal.2019;[Epub]     CrossRef
  • Ignorance may be Bliss (for Intensivists), but not for ICU Patients!
    Atul P. Kulkarni, Sumitra G Bakshi
    Indian Journal of Critical Care Medicine.2019; 23(4): 161.     CrossRef
Case Report
Vagal Reflex Induced Bronchospasm
Tae Hyeong Kim, Yong Lak Kim
Korean J Crit Care Med. 2000;15(2):113-116.
  • 2,017 View
  • 31 Download
AbstractAbstract PDF
The parasympathetic nervous system has been considered to have an important role in bronchospasm. Although vagal reflexes are well documented in animal models of airway hyperresponsiveness, their importance in asthmatic attacks in man is less documented. We report a case of bronchospasm during sclera buckling operation and we believe that this patient's bronchospasm was induced by the vagal reflex.
Original Article
The Effect of Clonidine Pretreatment on Bupivacaine-induced Cardiac Toxicity in Rabbit
Eun Ju Lee, Jin Young Chon, Yong Woo Choi, Se Ho Moon
Korean J Crit Care Med. 1998;13(2):205-211.
  • 1,491 View
  • 5 Download
AbstractAbstract PDF
BACKGOUND: Bupivacaine, an amide type local anesthetic, is frequently used for regional anesthesia. Bupivacaine overdose induces cardiac toxicity and directly depresses both cardiac electrophysiology and hemodynamic status. Clonidine, an imidazolin alpha-2-adrenoreceptor agonist, given prophylactically may delay the toxic manifestation of bupivacaine overdose and does not accentuate the subsequent hypotension. We studied the effect of clonidine pretreatment on bupivacaine induced cardiac toxicity.
METHODS
Fourteen rabbits (seven in each group) were anesthetized with ketamine and rompun, and tracheostomy was performed. Spontaneous ventilation with room air was continued throughout the experiment. Electrocardiogram, heart rate, and invasive arterial blood pressure were continuously recorded. Clonidine 5 microgram/kg (clonidine group) or saline (control group) was injected intravenously in randomized fashion. After 15 minutes, an intravenous infusion of bupivacaine was started at 0.3 mg/kg/min. The time of occurrence of the bupivacaine-induced toxic events: first dysrhythmia, 25% and 50% reduction in basal heart rate and mean arterial pressure, and asystole were recorded. At 5, 10, 15, and 20 minutes after bupivacaine infusion, 2 ml of whole blood were withdrawn via femoral arterial catheter for determination of bupivacaine concentration.
RESULTS
The threshold time at the first dysrhythmia was significantly greater in the clonidine group (27.2+/-4.5 min) than control group (19.9+/-1.2 min). The threshold times at the 25 and 50% reduction in basal heart rate were significantly greater in the clonidine group (23.7+/-5.8 min, 33.2+/-5.1 min) than control group (16.6+/-2.9 min, 22.9+/-2.8 min) and in basal mean arterial pressure were significantly greater in the clonidine group (15.6+/-2.6 min, 25.3+/-3.7 min) than control group (9.7+/-2.7 min, 16.3+/-5.8 min). The threshold time at the asystole was significantly greater in the clonidine group (38.2+/-7.7 min) than control group (28.7+/-3.4 min). At 5, 10, 15, and 20 minutes after bupivacaine infusion, there was no significant difference in the plasma bupivacaine concentration between two groups.
CONCLUSION
This study demonstrates that clonidine pretreatment delays the cardiac toxic manifestations of bupivacaine overdose. And plasma bupivacaine concentration was not influenced by clonidine pretreatment.
Case Report
Combination Therapy of Verapamil and Esmolol for the Paroxysmal Supraventricular Tachycardia Recurred during the Central Venous Catheterization: A case report
Eun Jung Kwon, Myoung Hoon Kong, Sang Ho Lim, Joon Hyeuk Choi, Mi Kyoung Lee, Suk Min Yoon, Young Seok Choi
Korean J Crit Care Med. 1997;12(1):81-84.
  • 1,808 View
  • 6 Download
AbstractAbstract PDF
Combination therapy of beta-blocker and a calcium channel blocker is not recommened because their additive effect on the myocardium and the atrioventricular node may precipitate heart block in susceptible patients. We experienced a 68 years old female patient who had paroxysmal supraventricular tachycardia that was treated with verapamil and esmolol. She had been taking verapamil for 2 years because of her paroxysmal supraventricular tachycardia. She was planned for left ureteronephrectomy due to left ureteral tumor. After epidural catheterization for the postoperative pain control, she was anesthetized with isoflurane and vecuronium. During central venous catheterization, SVT (H.R. from 98 beats per minute to 190 BPM) was suddenly developed with hypotension (B.P. from 120/65 mmHg to 75/42 mmHg) when guide wire was introduced. We treated her with combination therapy of verapamil 7.5 mg and esmolol 18 mg under the monitoring of blood pressure, electrocardiogram, end-tidal CO2 tension, central venous pressure and pulse oximeter. After 20 minutes of vigorous treatment, her heart rate and blood pressure returned to a normal range.

ACC : Acute and Critical Care