Tongue necrosis as a complication of vasoconstrictor agents in the intensive care setting

Noordally, S. Oaleed; Sohawon, Schoeb; Duttmann, Ruth; Gottignies, Philippe; Devriendt, Jacques

doi:10.1007/s11739-010-0416-3

Cited by 12 publications

(4 citation statements)

References 4 publications

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“…In clinical practice, it has been reported that raising MAP from 54 ± 8 to 77 ± 9 mm Hg with norepinephrine in patients with septic shock improved muscle (thenar eminence) oxygenation as measured by NIRS (23). It remains unclear why this did not agree with our results; however, tongue necrosis in the intensive care unit has been reported to be attributed to an overdose of vasoconstrictors (24). The liver showed a constant relationship between MAP and TOI, even during endotoxic shock, and vasopressor administration did not decrease oxygenation.…”

Section: Discussioncontrasting

confidence: 89%

Impact of high-dose vasopressor during endotoxic shock on the cerebral, lingual, hepatic, and renal microcirculation evaluated by near-infrared spectroscopy in swine

Kurita,

Kawashima,

Khaleelullah

et al. 2023

Shock

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Background High-dose vasopressors maintain blood pressure during septic shock but may adversely reduce microcirculation in vital organs. We assessed the effect of high-dose norepinephrine and vasopressin on the microcirculation of the brain, tongue, liver, and kidney during endotoxic shock using near-infrared spectroscopy (NIRS). Methods Thirteen pigs (24.5 ± 1.8 kg) were anesthetized, and an NIRS probe was attached directly to each organ. Approximately 0.2, 0.5, 1, and 2 μg/kg/min of norepinephrine were administered in a stepwise manner, followed by 0.5, 1, 2, and 5 μg/kg/min of sodium nitroprusside in normal condition. Moreover, 1 μg/kg/h of lipopolysaccharide was administered continuously after 100 μg bolus to create endotoxic shock, and after 1000 mL of crystalloid infusion, high-dose norepinephrine (2, 5, 10, and 20 μg/kg/min) and vasopressin (0.6, 1.5, 3, and 6 U/min) were administered in a stepwise manner. The relationship between the mean arterial pressure (MAP) and each tissue oxygenation index (TOI) during vasopressor infusion was evaluated. Results Three pigs died after receiving lipopolysaccharides, and 10 were analyzed. An increase of >20% from the baseline MAP induced by high-dose norepinephrine during endotoxic shock reduced the TOI in all organs except the liver. The elevation of MAP to baseline with vasopressin alone increased the kidney and liver TOIs and decreased the tongue TOI. Conclusions Forced blood pressure elevation with high-dose norepinephrine during endotoxic shock decreased the microcirculation of vital organs, especially the kidney. Cerebral TOI may be useful for identifying the upper limit of blood pressure, at which norepinephrine impairs microcirculation.

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Section: Discussioncontrasting

confidence: 89%

Impact of high-dose vasopressor during endotoxic shock on the cerebral, lingual, hepatic, and renal microcirculation evaluated by near-infrared spectroscopy in swine

Kurita,

Kawashima,

Khaleelullah

et al. 2023

Shock

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“…In cases where a conservative approach is adopted the necrotic tissue will demarcate and autoamputate over time. Healing in this instance is by secondary intention and may lead to considerable deformity and issues with speech and swallowing 2. Ultimately, the correlation between extensive lingual necrosis and other severe co-morbidities, resulting in end-organ damage, may highlight a poor overall prognosis.…”

Section: Discussionmentioning

confidence: 99%

Ischaemic necrosis of the tongue

McGoldrick¹,

Khan

Cotter

2015

BMJ Case Reports

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Necrosis of the tongue is a rare clinical finding. The rich vascularity of the tongue means necrosis is uncommon but it has been reported secondary to giant cell arthritis, radiotherapy and ischaemia. We report the case of a 61-year-old man admitted with an acute abdomen, who later developed gross swelling of the tongue, secondary to ischaemic necrosis, which necessitated tracheostomy placement. The ischaemia was managed conservatively with heparinisation and by allowing the ischaemic area to demarcate and slough off naturally.

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“…There are many underlying factors that can contribute to the development of tongue necrosis (Table 1 ). 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 Giant cell arteritis (GCA), ANCA (Anti‐Neutrophil Cytoplasmic Antibody)‐associated vasculitis and other vasculitides have been previously described as underlying systemic causes of tongue necrosis. 1 , 2 , 3 , 4 Other potential causes include infection (particularly tuberculosis and syphilis), malignancy, radiation therapy, use of vasoconstricting medications and systemic hypoperfusion such as in the setting of shock.…”

Section: Introductionmentioning

confidence: 99%

Tongue necrosis as a manifestation of immune dysfunction: A complex case of systemic lupus erythematosus, histoplasmosis, and macrophage activation syndrome

Walsh

Feng

Lenert

et al. 2023

Clinical Case Reports

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Tongue necrosis as a complication of vasoconstrictor agents in the intensive care setting

Cited by 12 publications

References 4 publications

Impact of high-dose vasopressor during endotoxic shock on the cerebral, lingual, hepatic, and renal microcirculation evaluated by near-infrared spectroscopy in swine

Impact of high-dose vasopressor during endotoxic shock on the cerebral, lingual, hepatic, and renal microcirculation evaluated by near-infrared spectroscopy in swine

Ischaemic necrosis of the tongue

Tongue necrosis as a manifestation of immune dysfunction: A complex case of systemic lupus erythematosus, histoplasmosis, and macrophage activation syndrome

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