In For A Penny, In For a Pound
Answer: B
This woman presents with (as of yet) undifferentiated shock – you shift your focus now to rapid assessment and intervention.
The four main categories of shock may be remembered by this memory aid:
“How they ‘COHDe’:
Cardiogenic
Obstructive,
Hypovolemic
Distributive
e
The history you cobble together from various sources and your clinical exam are your guide to the etiology of shock. Ultrasound can augment or confirm your assessment:
http://www.ncbi.nlm.nih.gov/pubmed/19945597
http://emcrit.org/wp-content/uploads/2011/03/New-RUSH-Review-Article1.pdf
Epidemiologically speaking, distributive shock in the form of sepsis syndrome is the most common type (64%; non-septic distributive shock, 4%), followed by hypovolemic (16%) and cardiogenic (16%); obstructive shock is uncommon (2%).
This woman presents with (as of yet) undifferentiated shock – you shift your focus now to rapid assessment and intervention.
The four main categories of shock may be remembered by this memory aid:
“How they ‘COHDe’:
Cardiogenic
Obstructive,
Hypovolemic
Distributive
e
The history you cobble together from various sources and your clinical exam are your guide to the etiology of shock. Ultrasound can augment or confirm your assessment:
http://www.ncbi.nlm.nih.gov/pubmed/19945597
http://emcrit.org/wp-content/uploads/2011/03/New-RUSH-Review-Article1.pdf
Epidemiologically speaking, distributive shock in the form of sepsis syndrome is the most common type (64%; non-septic distributive shock, 4%), followed by hypovolemic (16%) and cardiogenic (16%); obstructive shock is uncommon (2%).
(Vincent and de Backer, 2013)
It is important to note that these broad categories are not mutually exclusive. A classic example is sepsis: septic shock may be a combination of distributive (inflammatory mediators and poor cellular metabolism cause peripheral dilation), hypovolemic (insensible or active fluid losses), and potentially cardiogenic (inflammatory-mediated dysrhythmias, myocardial stunning, or demand ischemia) etiologies.
Adequate and rapid fluid resuscitation is essential (even in the case of suspected cardiogenic shock, an initial bolus may be beneficial and will help to guide further therapy).
Three physiologic “windows” to circulation are available to the clinician at the bedside:
Skin: cold, clammy, with faint pulses; or warm, with flash capillary refill and bounding pulses?
Neurologic: confusion, obtundation, or stupor?
Renal: decreased urine output (concentrated urine by history or < 0.5 mL/kg/h)?
A serum lactate is a good adjunct to detect occult hypoperfusion states.
Although some patients will respond with fluids only, many need some vasoactive support of their blood pressure to ensure vital organ perfusion.
From a practical standpoint, the question arises: what vasopressors can I use in my peripheral line?
This is a subject of much clinician consternation, charged by a plethora of anecdote and a paucity of evidence: case reports and retrospective case series frame the discussion.
Although there are case reports of soft tissue complications of all the above vasopressors, norepinephrine (B), an alpha-adrenergic agonist, is probably the most feared agent to use peripherally; inadvertent extravasation can cause significant tissue necrosis:
It is important to note that these broad categories are not mutually exclusive. A classic example is sepsis: septic shock may be a combination of distributive (inflammatory mediators and poor cellular metabolism cause peripheral dilation), hypovolemic (insensible or active fluid losses), and potentially cardiogenic (inflammatory-mediated dysrhythmias, myocardial stunning, or demand ischemia) etiologies.
Adequate and rapid fluid resuscitation is essential (even in the case of suspected cardiogenic shock, an initial bolus may be beneficial and will help to guide further therapy).
Three physiologic “windows” to circulation are available to the clinician at the bedside:
Skin: cold, clammy, with faint pulses; or warm, with flash capillary refill and bounding pulses?
Neurologic: confusion, obtundation, or stupor?
Renal: decreased urine output (concentrated urine by history or < 0.5 mL/kg/h)?
A serum lactate is a good adjunct to detect occult hypoperfusion states.
Although some patients will respond with fluids only, many need some vasoactive support of their blood pressure to ensure vital organ perfusion.
From a practical standpoint, the question arises: what vasopressors can I use in my peripheral line?
This is a subject of much clinician consternation, charged by a plethora of anecdote and a paucity of evidence: case reports and retrospective case series frame the discussion.
Although there are case reports of soft tissue complications of all the above vasopressors, norepinephrine (B), an alpha-adrenergic agonist, is probably the most feared agent to use peripherally; inadvertent extravasation can cause significant tissue necrosis:
(Kim et al, 2012)
In a systematic review, Loubani et al. reviewed 79 reported cases of skin and soft tissue complications following vasopressor use: 11 (14%) were in the context of central administration and 68 (86%) with peripheral administration. In the 68 cases of peripheral vasopressor administration, the problematic peripheral line
used was most often in the foot (55%) and for prolonged periods of time (88% had vasopressor administration longer than 6 hours, with 69% longer than 24 hours). Norepinephrine was the vasopressor most commonly implicated in skin complications from peripheral administration (37/68, 54% of cases).
In a recent randomized control trial in three French ICUs (open-label, crossover-enabled), Ricard et al. compared complication rates in central and peripheral venous access. The “primary” endpoint, unfortunately was a list of
endpoints; when they compared rates of cases without “any” complication, the central venous group included 86/135 and the peripheral venous group included 67/128 cases, without statistical significance (P = 0.06).
Subgroups included soft tissue complications in both groups, but as the study was not powered to assess the differences, we will not outline them here. This study may help future researchers in planning more structured
studies.
In the ED the practice of many clinicians is to allow for peripheral administration of drugs such as dopamine (A), epinephrine (C), and vasopressin (D) through a large-bore IV with the intention of using this route as a temporary bridge to central venous administration. Some may avoid even short courses of norepinephrine peripherally, but this does not appear to be supported by the evidence. The key points are awareness of the possibility of complications (even if given centrally) and vigilance during their use.
This subject is a good example of the maxim “absence of evidence is not evidence of absence”. At this point, we still have a few things to guide our decisions in the initial management of the patient in shock needing a vasopressor but currently with only intravenous access: our knowledge of pharmacology, our awareness of case reports, and our charge to offer our patients the best possible balance of risk-to-benefit ratio in a given circumstance.
References
Berben JY, Bryant MF, Howard JM. Etiology and prevention of sloughs produced by L-norepinephrine (levophed). Ann Surg. 1957 Dec;146(6):1016-20.
Bunker N, Higgins D. Peripheral administration of vasopressin for catecholamine-resistant hypotension complicated by skin necrosis. Crit Care Med. 2006 Mar;34(3):935; author reply 935-6.
Chen JL, O'Shea M. Extravasation injury associated with low-dose dopamine. Ann Pharmacother. 1998 May;32(5):545-8.
Dugger B. Peripheral dopamine infusions: are they worth the risk of infiltration? J Intraven Nurs. 1997 Mar-Apr;20(2):95-9.
Kahn JM, Kress JP, Hall JB. Skin necrosis after extravasation of low-dose vasopressin administered for septic shock. Crit Care Med. 2002 Aug;30(8):1899-901.
Kim SM, Aikat S, Bailey A. Well recognised but still overlooked: norepinephrine extravasation. BMJ Case Reports.
2012; doi:10.1136/bcr-2012-006836.
Ricard JD, Salomon L, Boyer A, Thiery G, Meybeck A, Roy C, Pasquet B, Le Mière E, Dreyfuss D. Central or peripheral catheters for initial venous access of ICU patients: a randomized controlled trial. Crit Care Med. 2013 Sep;41(9):2108-15. doi: 10.1097/CCM.0b013e31828a42c5.
Vincent J, De Backer D. Circulatory Shock. N Engl J Med. 2013;369:1726-34. DOI:10.1056/NEJMra1208943.
In a systematic review, Loubani et al. reviewed 79 reported cases of skin and soft tissue complications following vasopressor use: 11 (14%) were in the context of central administration and 68 (86%) with peripheral administration. In the 68 cases of peripheral vasopressor administration, the problematic peripheral line
used was most often in the foot (55%) and for prolonged periods of time (88% had vasopressor administration longer than 6 hours, with 69% longer than 24 hours). Norepinephrine was the vasopressor most commonly implicated in skin complications from peripheral administration (37/68, 54% of cases).
In a recent randomized control trial in three French ICUs (open-label, crossover-enabled), Ricard et al. compared complication rates in central and peripheral venous access. The “primary” endpoint, unfortunately was a list of
endpoints; when they compared rates of cases without “any” complication, the central venous group included 86/135 and the peripheral venous group included 67/128 cases, without statistical significance (P = 0.06).
Subgroups included soft tissue complications in both groups, but as the study was not powered to assess the differences, we will not outline them here. This study may help future researchers in planning more structured
studies.
In the ED the practice of many clinicians is to allow for peripheral administration of drugs such as dopamine (A), epinephrine (C), and vasopressin (D) through a large-bore IV with the intention of using this route as a temporary bridge to central venous administration. Some may avoid even short courses of norepinephrine peripherally, but this does not appear to be supported by the evidence. The key points are awareness of the possibility of complications (even if given centrally) and vigilance during their use.
This subject is a good example of the maxim “absence of evidence is not evidence of absence”. At this point, we still have a few things to guide our decisions in the initial management of the patient in shock needing a vasopressor but currently with only intravenous access: our knowledge of pharmacology, our awareness of case reports, and our charge to offer our patients the best possible balance of risk-to-benefit ratio in a given circumstance.
References
Berben JY, Bryant MF, Howard JM. Etiology and prevention of sloughs produced by L-norepinephrine (levophed). Ann Surg. 1957 Dec;146(6):1016-20.
Bunker N, Higgins D. Peripheral administration of vasopressin for catecholamine-resistant hypotension complicated by skin necrosis. Crit Care Med. 2006 Mar;34(3):935; author reply 935-6.
Chen JL, O'Shea M. Extravasation injury associated with low-dose dopamine. Ann Pharmacother. 1998 May;32(5):545-8.
Dugger B. Peripheral dopamine infusions: are they worth the risk of infiltration? J Intraven Nurs. 1997 Mar-Apr;20(2):95-9.
Kahn JM, Kress JP, Hall JB. Skin necrosis after extravasation of low-dose vasopressin administered for septic shock. Crit Care Med. 2002 Aug;30(8):1899-901.
Kim SM, Aikat S, Bailey A. Well recognised but still overlooked: norepinephrine extravasation. BMJ Case Reports.
2012; doi:10.1136/bcr-2012-006836.
Ricard JD, Salomon L, Boyer A, Thiery G, Meybeck A, Roy C, Pasquet B, Le Mière E, Dreyfuss D. Central or peripheral catheters for initial venous access of ICU patients: a randomized controlled trial. Crit Care Med. 2013 Sep;41(9):2108-15. doi: 10.1097/CCM.0b013e31828a42c5.
Vincent J, De Backer D. Circulatory Shock. N Engl J Med. 2013;369:1726-34. DOI:10.1056/NEJMra1208943.