PERSPECTIVES

ANZJSurg.com

Vital signs are unreliable

In the initial encounter with a trauma victim in the eld, the paramedic must rapidly assess the patient and make triage decisions based on the likelihood of major injury. Undertriage is a signicant problem as initial transport of a major trauma victim to a non-trauma centre (NTC) rather than a designated trauma centre is signicantly associated with up to 3.8 times greater odds of mortality.15 In a large study of severely injured blunt trauma victims, 29% were initially inappropriately triaged to an NTC.1 Unrecognized shock is not restricted to the pre-hospital setting, though; this problem is just as likely in the emergency department (ED), the operating room, the intensive care unit (ICU) and the hospital ward. The traditional model of haemorrhagic shock holds that as bleeding ensues, derangement of vital signs progresses in an orderly, step-wise fashion. Hence, patients with normal vital signs are stable and assumed to be without serious injuries while those with abnormal vital signs require immediate attention. In reality, this is not necessarily the case. Over eons of evolution, nature has designed our bodies to compensate for blood loss such that changes in vital signs often do not change until a critical stage. The classication system of shock commonly taught by the Advanced Trauma Life Support (ATLS) course is overly simplistic and its continued use may be counterproductive by relaxing the sense of urgency in a patient with normal vital signs. Conventional teaching states that tachycardia is an early sign of blood loss as the compensatory increase in heart rate (HR) is fundamental to the physiologic response to haemorrhage. In practice, HR is extremely inaccurate as a triage tool to predict the need for operations, need for massive transfusions and mortality.6,7 In a retrospective review of penetrating abdominal injuries and severe isolated extremity trauma, Thompson et al. report that fully 45.8% of hypotensive patients were found to be inappropriately bradycardic.8 Furthermore, in the subset with >1.0 L intraoperative blood loss, 21% were not tachycardic. More recently, Ley et al. reported that not only is relative bradycardia common (45%) in hypotensive patients, but it is associated with signicantly higher mortality.9 With a concomitant brain injury, bradycardia will also complicate the clinical picture. Systolic blood pressure (SBP), the most frequently referenced vital sign, is particularly well compensated, and derangement is usually a late nding.10 In a study of injured patients requiring emergency thoracoabdominal surgery and >5 units of packed red blood cells transfusion, fully one-third arrived in the ED with a normal blood pressure (>120 mm Hg).11 The SBP cut-off of <90 mm Hg (recommended by the American College of Emergency Physicians and American College of Surgeons) is based on very little scientic evidence. In recent years, multiple studies have reported that mortality signicantly increases at an inection point of 110 mm Hg.1214 Intoxicating substances such as alcohol, cocaine and amphetamines, present in up to 70% of trauma victims,15 are well known to affect SBP and HR, providing false security to inexperienced providers. The stress response to pain, fear, anger and agitation further confounds the clinical picture. The elderly trauma patient, the most rapidly growing segment of the US population, presents additional challenges to pre-hospital providers for several reasons. Firstly, one must account for the normal effects of aging. It is well established that increasing age is associated with an upward trend in SBP such that the normal blood pressure required for vital organ perfusion is necessarily higher. Compounding this problem is the co-morbidity of essential hypertension, a medical illness present in up to 79% of the elderly population.16 As an example, a 62-year-old man with a measured blood pressure of 120 mm Hg may normally live at a SBP of 160 mm Hg. In a younger patient with a similar decline in pressure D 40 mm Hg from normal (e.g. 70 mm Hg from 110 mm Hg), there is no question of the gravity of the situation. Even with a normal presenting blood pressure, geriatric mortality rates are 9- to 10-fold higher than for younger patients.17 An elderly patient may be in unrecognized clinical shock because of a falsely reassuring normal measured blood pressure, leading to inappropriate undertriage, delay in work-up, resuscitation and treatment. In multiple studies at the statewide and national level, elderly trauma victims are consistently undertriaged to NTC more frequently compared with their younger counterparts despite meeting physiology criteria.1820 Secondly, the HR, already an insensitive marker, is especially inaccurate in the elderly population because the aged heart has often lost the ability to compensate for hypovolaemia through tachycardia. Further confounding this problem is the common presence of disease-modifying medications such as b-blockers, which may further blunt the tachycardic response in shock. About one in ve elderly trauma patients are taking b-blockers.21 Lactic acid, produced during inadequate tissue perfusion, has been conclusively shown to be a robust prognosticator of outcome in shock when measured in the hospital setting. Indeed, several authors report that an elevated lactate can accurately distinguish survivors from non-survivors in normotensive patients.22,23 Others report that ED lactate is superior to traditional vital signs (TVSs) in predicting the need for blood transfusion, ICU resources, hospital stay and mortality.24,25 Rapid (60 s) point-of-care analyzers (cost: $231) that require only a single drop of blood (test strip: $1.80)26 have been proven accurate27 and reproducible and pilot studies in the prehospital setting are encouraging.28 Another alternative triage tool currently under investigation is the shock index (SI), dened as HR divided by SBP. The normal value is between 0.5 and 0.7. This easily calculated value shows a
2012 The Authors ANZ Journal of Surgery 2012 Royal Australasian College of Surgeons

ANZ J Surg 82 (2012) 574577

Perspectives

575

promise in detecting subtle alterations in TVS in the early stages of shock when the TVSs are still considered normal. Initial studies in healthy blood donors reported signicant elevation in SI despite HR and SBP within normal limits.29 Several authors have concluded that SI, whether calculated in the pre-hospital or ED setting, is more accurate than TVS at predicting need for massive blood transfusion and mortality.3032 It must be emphasized, however, that the SI data are predominantly retrospective, and prospective validation is required before widespread application can be recommended. In conclusion, the common trauma triage criteria used in ATLS and most EMS systems (formulated on expert opinion) are in need of revision and update to reect real-life data-driven trends. Alternative markers such as serum lactate levels and SI show a promise for identifying patients in preclinical shock. Currently, the best tool for diagnosing a patient in shock is the clinical acumen of an experienced clinician who considers many other factors such as mechanism of injury, injury patterns, laboratory abnormalities and response to volume. Sole reliance upon TVS in the evaluation of trauma victims will necessarily result in undertriage of patients in early shock. References
1. Nirula R, Maier R, Moore E, Sperry J, Gentilello L. Scoop and run to the trauma center or stay and play at the local hospital: hospital transfers effect on mortality. J. Trauma 2010; 69: 5959; discussion 599601. 2. Haas B, Gomez D, Zagorski B, Stukel TA, Rubenfeld GD, Nathens AB. Survival of the ttest: the hidden cost of undertriage of major trauma. J. Am. Coll. Surg. 2010; 211: 80411. 3. Pracht EE, Langland-Orban B, Flint L. Survival advantage for elderly trauma patients treated in a designated trauma center. J. Trauma 2011; 71: 6977. 4. Sampalis JS, Denis R, Frechette P, Brown R, Fleiszer D, Mulder D. Direct transport to tertiary trauma centers versus transfer from lower level facilities: impact on mortality and morbidity among patients with major trauma. J. Trauma 1997; 43: 28895; discussion 2956. 5. MacKenzie EJ, Rivara FP, Jurkovich GJ et al. A national evaluation of the effect of trauma-center care on mortality. N. Engl. J. Med. 2006; 354: 36678. 6. Brasel KJ, Guse C, Gentilello LM, Nirula R. Heart rate: is it truly a vital sign? J. Trauma 2007; 62: 8127. 7. Demetriades D, Chan LS, Bhasin P et al. Relative bradycardia in patients with traumatic hypotension. J. Trauma 1998; 45: 5349. 8. Thompson D, Adams SL, Barrett J. Relative bradycardia in patients with isolated penetrating abdominal trauma and isolated extremity trauma. Ann. Emerg. Med. 1990; 19: 26875. 9. Ley EJ, Salim A, Kohanzadeh S, Mirocha J, Margulies DR. Relative bradycardia in hypotensive trauma patients: a reappraisal. J. Trauma 2009; 67: 10514. 10. Parks JK, Elliott AC, Gentilello LM, Sha S. Systemic hypotension is a late marker of shock after trauma: a validation study of Advanced Trauma Life Support principles in a large national sample. Am. J. Surg. 2006; 192: 72731. 11. Luna GK, Eddy AC, Copass M. The sensitivity of vital signs in identifying major thoracoabdominal hemorrhage. Am. J. Surg. 1989; 157: 5125.

12. Bruns B, Gentilello L, Elliott A, Sha S. Prehospital hypotension redened. J. Trauma 2008; 65: 121721. 13. Eastridge BJ, Salinas J, McManus JG et al. Hypotension begins at 110 mm Hg: redening hypotension with data. J. Trauma 2007; 63: 2917; discussion 2979. 14. Edelman DA, White MT, Tyburski JG, Wilson RF. Post-traumatic hypotension: should systolic blood pressure of 90109 mm Hg be included? Shock 2007; 27: 1348. 15. Madan AK, Yu K, Beech DJ. Alcohol and drug use in victims of lifethreatening trauma. J. Trauma 1999; 47: 56871. 16. Gangavati A, Hajjar I, Quach L et al. Hypertension, orthostatic hypotension, and the risk of falls in a community-dwelling elderly population: the maintenance of balance, independent living, intellect, and zest in the elderly of Boston study. J. Am. Geriatr. Soc. 2011; 59: 3839. 17. Heffernan DS, Thakkar RK, Monaghan SF et al. Normal presenting vital signs are unreliable in geriatric blunt trauma victims. J. Trauma 2010; 69: 81320. 18. Phillips S, Rond PC, Kelly SM, Swartz PD. The failure of triage criteria to identify geriatric patients with trauma: results from the Florida Trauma Triage Study. J. Trauma 1996; 40: 27883. 19. Ryb GE, Dischinger PC. Disparities in trauma center access of older injured motor vehicular crash occupants. J. Trauma 2011; 71: 7427. 20. Ma MH, MacKenzie EJ, Alcorta R, Kelen GD. Compliance with prehospital triage protocols for major trauma patients. J. Trauma 1999; 46: 16875. 21. Neideen T, Lam M, Brasel KJ. Preinjury beta blockers are associated with increased mortality in geriatric trauma patients. J. Trauma 2008; 65: 101620. 22. Callaway DW, Shapiro NI, Donnino MW, Baker C, Rosen CL. Serum lactate and base decit as predictors of mortality in normotensive elderly blunt trauma patients. J. Trauma 2009; 66: 10404. 23. Paladino L, Sinert R, Wallace D, Anderson T, Yadav K, Zehtabchi S. The utility of base decit and arterial lactate in differentiating major from minor injury in trauma patients with normal vital signs. Resuscitation 2008; 77: 3638. 24. Vandromme MJ, Grifn RL, Weinberg JA, Rue LW, Kerby JD. Lactate is a better predictor than systolic blood pressure for determining blood requirement and mortality: could prehospital measures improve trauma triage? J. Am. Coll. Surg. 2010; 210: 8617; 8679. 25. Lavery RF, Livingston DH, Tortella BJ, Sambol JT, Slomovitz BM, Siegel JH. The utility of venous lactate to triage injured patients in the trauma center. J. Am. Coll. Surg. 2000; 190: 65664. 26. Brinkert W, Rommes JH, Bakker J. Lactate measurements in critically ill patients with a hand-held analyser. Intensive Care Med. 1999; 25: 9669. 27. Slomovitz BM, Lavery RF, Tortella BJ, Siegel JH, Bachl BL, Ciccone A. Validation of a hand-held lactate device in determination of blood lactate in critically injured patients. Crit. Care Med. 1998; 26: 15238. 28. Jansen TC, van Bommel J, Mulder PG, Rommes JH, Schieveld SJ, Bakker J. The prognostic value of blood lactate levels relative to that of vital signs in the pre-hospital setting: a pilot study. Crit. Care 2008; 12: R160. 29. Birkhahn RH, Gaeta TJ, Terry D, Bove JJ, Tloczkowski J. Shock index in diagnosing early acute hypovolemia. Am. J. Emerg. Med. 2005; 23: 3236. 30. Vandromme MJ, Grifn RL, Kerby JD, McGwin G, Rue LW, Weinberg JA. Identifying risk for massive transfusion in the relatively normotensive patient: utility of the prehospital shock index. J. Trauma 2011; 70: 38490.

2012 The Authors ANZ Journal of Surgery 2012 Royal Australasian College of Surgeons

576

Perspectives

31. Zarzaur BL, Croce MA, Fischer PE, Magnotti LJ, Fabian TC. New vitals after injury: shock index for the young and age x shock index for the old. J. Surg. Res. 2008; 147: 22936. 32. Zarzaur BL, Croce MA, Magnotti LJ, Fabian TC. Identifying lifethreatening shock in the older injured patient: an analysis of the National Trauma Data Bank. J. Trauma 2010; 68: 11348.

Daniel Dante Yeh, MD George C. Velmahos, MD, PhD Department of Surgery, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts, USA doi: 10.1111/j.1445-2197.2012.06171.x

Functional axillary anatomy: time for a new look at the clavipectoral fascia?
The breast is derived from the ectoderm and develops between the supercial and deep layers of the supercial fascia. Its lymphatics form a complex network of periductal and perilobular vessels, these come to lie alongside the lactiferous ducts as they converge at the nipple and empty into the subareolar plexus of Sappey. In addition, these intraparenchymal lymphatics are linked to vessels within the dermis. Tributaries from this nexus condense into two large trunks (vasa lymphatica mammaria magna) which course supercially to the lower axillary lymph nodes. The lymphatic drainage patterns, through the axilla, from this point are less well dened. The breast skin envelope and underlying glandular tissue therefore share a common lymphatic pathway to axillary sentinel nodes. This anatomical model is largely derived from the publications of Sappey in the 1870s. The neo-Halstedian idea of sentinel node biopsy is also predicated on this hypothesis and has become the standard of care in the management of clinically node negative breast cancer. Axillary dissection still has the well known risk of arm lymphoedema with therapies for control but no cure.1 Elegant anatomical studies have begun to outline the greater complexity of the breast lymphatics and the role of perforating lymphatics related to fascial planes has been described.2 The clavipectoral fascia is a distinct axillary feature but has largely been ignored in modern descriptions of axillary anatomy. Anatomy textbooks still describe it as a single coronal layer enveloping the axillary vein, subclavius muscle, and producing the hollow of the axilla by its inferior attachments. Halsteds ligament is probably a derivative of this fascia and marks the highest point of level III. It is, however, a laminated, complex, three-dimensional structure. Its laminations are routinely seen during axillary insonation. There are three to four anterior layers and these are often depicted in radiology textbooks without comment.3 This is evident at surgery when performing an axillary dissection. During the course of this operation, several clavipectoral fascial layers have to be divided longitudinally along the lateral edge of pectoralis minor. A loose areolar tissue plane lateral to the serratus fascia is then entered to nd the posteriorly situated long thoracic nerve. The clavipectoral fascia is then divided transversely to expose the axillary vein. Deep to this layer, a thinner fascial lamina has to be divided to expose the thoracodorsal neurovascular bundle. Further dissection of the axilla leaves a medial sagittal sheet of fascia that can be grasped between the nger and the thumb. This structure extends towards the medial part of the axillary vein and the apex of the axilla. The main motor nerves are seen on either side of this tissue, hence the term interneural tissue. Breast surgeons excise this sheet near the oor of the axilla. It has been shown to be rich in lymphatic tissue.4 The anterior coronal clavipectoral fascial layer is clearly a multilaminated structure and the condensations and reections of these laminae give rise to the fascial structures described above. The intriguing question is whether these compartmentalizations segment the axilla and have a role in segregating breast and arm lymphatic ow. Sentinel node biopsy has certainly increased our understanding of axillary lymphatic anatomy.5,6 The vast majority of breast axillary sentinel nodes are found in the medial axilla and have been related to the lateral thoracic vein or second intercostal nerve.5,7 The relationship of the sentinel nodes, their afferent, efferent and perforating tracts to the clavipectoral fascia and its derivatives, has not been described and awaits elucidation. The microvascular dissection and imaging techniques that could study this further have been formulated and should be encouraged.2,8 Reverse axillary mapping has given us further clues about axillary lymphatic ow if blue dye is injected into the arm, the bluecoloured lymphatics are visible through the sentinel node biopsy incision.9,10 The arm lymph nodes appear to be largely separate, in a different eld, from the breast sentinel nodes. While there may be cross-connections and alteration by metastases, breast and arm lymphatic ow seems to be segregated. This may mean that if only breast nodes can be removed, usually from the medial axilla lymphoedema rates can be reduced. The subdivisions and threedimensional anatomy of the clavipectoral fascia may add to this knowledge. A fuller description of the complete axillary lymphatic and fascial anatomy holds the exciting prospect of understanding why some patients get arm lymphoedema after surgical clearance and some do not. Further renements of axillary surgery with this knowledge may improve outcomes for affected patients. References
1. Benson JR, della Rovere GQ. Management of the axilla in women with breast cancer. Lancet Oncol. 2007; 8: 33148. 2. Suami H, Pan WR, Mann GB, Taylor GI. The lymphatic anatomy of the breast and its implications for sentinel lymph node biopsy: a human cadaver study. Ann. Surg. Oncol. 2008; 15: 86371. 3. Stavros AT. Breast Ultrasound. Philadelphia: Lippincott Williams and Wilkins, 2004; 843 p.

2012 The Authors ANZ Journal of Surgery 2012 Royal Australasian College of Surgeons