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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 6  |  Issue : 4  |  Page : 247-250

Central venous pressure as end-point fluid removal in drowning patients: A case report


Department of Anesthesiology and Intensive Care, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia

Date of Submission15-Aug-2022
Date of Decision25-Sep-2022
Date of Acceptance05-Oct-2022
Date of Web Publication31-Oct-2022

Correspondence Address:
Eka Yudha Lantang
Department of Anesthesiology and Intensive Care, Faculty of Medicine, Universitas Indonesia, Jl. Salemba Raya No. 6, Kenari, Kec. Senen, Kota Jakarta Pusat, Daerah Khusus Ibu Kota, Jakarta 10430
Indonesia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bjoa.bjoa_210_22

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  Abstract 

Central venous pressure (CVP) is used as a guidance to control hemodynamics and to achieve the efficacy of hemodynamic balance. The drowning patient experienced a laryngeal spasm, which caused water passively enter the respiratory tract and accumulated in the lungs. Excess fluid in the lungs leads to pulmonary hypertension, venous congestion, and increased CVP. The use of diuretics guided by CVP values is the best way to achieve hemodynamic balance. Two drowning patients in different water had an increased CVP up to 12 mmHg in the sea, with serum creatinine (sCr) of 0.5 mg/dL and cumulative fluid balance (CFB) of −250 cc, and others in the lake CVP up to 14 mmHg with sCr of 0.7 mg/dL and CFB of −320 cc. Both were given furosemide at a dose of 5 mg from the first day of treatment until day 5 when both patients’ CVP returned to normal values, CVP of 5 mmHg, sCr of 0.6 mg/dL, and CFB of −1105 cc, and the others with CVP of 1 mmHg, sCr of 0.6, and CFB of −1170, then furosemide was discontinued. The use of furosemide with CVP guidance shows effective results in reducing fluids and venous congestion and is safe for the kidney, which is marked by normal values of sCr and CFB.

Keywords: Central venous pressure, creatinine, cumulative fluid balance, furosemide, hemodynamics


How to cite this article:
Lantang EY, George Y, Sugiarto A, Diana A. Central venous pressure as end-point fluid removal in drowning patients: A case report. Bali J Anaesthesiol 2022;6:247-50

How to cite this URL:
Lantang EY, George Y, Sugiarto A, Diana A. Central venous pressure as end-point fluid removal in drowning patients: A case report. Bali J Anaesthesiol [serial online] 2022 [cited 2022 Nov 26];6:247-50. Available from: https://www.bjoaonline.com/text.asp?2022/6/4/247/359934




  Introduction Top


Drowning is one of the most common causes of death in the world. In some cases of drowning, the victim will experience a laryngeal spasm as an automatic response to the respiratory reflex and will lead to fatal complications because of persistent spasms. Consequently, there is a decrease in consciousness and causes water to enter passively into the respiratory tract, and the process continues with heart rhythm disturbances, which will be followed by tachycardia and bradycardia to pulseless electrical activity, and finally asystole. When water enters the breath, it will cause a buildup of fluid in the lungs and cause acute pulmonary edema.[1] Excess fluid in the lungs triggers pulmonary hypertension and venous congestion. Venous congestion that causes a greater outflow of oncotic pressure will cause peripheral edema or an increase in central venous pressure (CVP).[2]

Fluid removal using diuretics is the mainstay of treatment in reducing congestion and fluid in the early postresuscitation phase of shock patients. The use of CVP as a guide for hemodynamic control in the body is the best way to achieve the efficacy of hemodynamic balance. The best balance is achieved by reducing intravascular hydrostatic pressure without reducing venous return and stroke volume or cardiac output.[3]


  Case Report Top


Case 1

A 27-year-old man was brought to the Emergency Department, referred from a private hospital with the chief complaints of loss of consciousness due to drowning on the beach about 3 h before admission to the hospital. The general state was a severe illness, unresponsive awareness (with AVPU scale), blood pressure of 69/48 mmHg, pulse rate of 122 times/min, respiratory rate of 38×/min with the saturation of 78%, and crackles on auscultation of both lung fields. About 1 h before, the patient consumed alcohol. The patient was not given cardiopulmonary resuscitation, while at the scene or at the first hospital the victim arrived [Chart 1].
Chart 1: The changes of CVP, creatinine, and CFB in case 1. CFB = cumulative fluid balance, CVP = central venous pressure

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The patient was intubated and mechanically ventilated with an initial PC mode of 15/14/7/100%. It was decided to give noradrenaline titration starting at 0.05 mcg/kg BW/min through peripheral venous access, the patient’s CVP was 12 mmHg, furosemide 5 mg, and ceftriaxone 1 g/24 h. An initial 300 cc of urine was obtained.

The administration of furosemide was continued in the intensive care unit (ICU) with monitoring of CVP. After 24 h of ICU treatment, the patient showed improvement. CVP decreased to 10 mmHg; rhonchi in both lung fields began to decrease from before and obtained a urine output of 1.5 mL/kg BW/h, a creatinine value of 1.4 mg/dL, and a negative cumulative fluid balance (CFB) of 250.

Oxygenation, administration of norepinephrine, diuretics, and antibiotics are maintained. On the third day of treatment, the patient began to improve, consciousness increased, GCS 9, CVP decreased (originally 10–12 mmHg to 6–8 mmHg), crackles disappeared, urine output was 0.7 mL/kg BW/h, with negative fluid balance cumulative of 955, and the urea creatinine value was within normal limits, and furosemide was discontinued. On day 5, the patient was checked for serum creatinine (sCr), 0.6 mg/dL. On the last day of treatment, day 6, the patient experienced full consciousness, GCS score of 15, CVP decreased by 2–4 mmHg, and urine output was 0.7 mL/kg BW/h with a negative CFB of 1045.

Case 2

A 23-year-old man was referred from a private hospital with the chief complaint of shortness of breath due to drowning in the lake about 6 h before entering the hospital, about 15 min of drowning. The general state was a severe illness, consciousness GCS E4M6V5, blood pressure of 114/110 mmHg, pulse rate of 133 beats/min, respiratory rate of 35×/min with a saturation of 92%, and the impression of pulmonary edema on auscultation of both lung fields, and accompanied by slight frosty sputum and debris, algae/lake plants in the mouth area. The patient is not given cardiopulmonary resuscitation at the scene or at the first hospital [Chart 2].
Chart 2: The changes of CVP, creatinine, and CFB in case 2. CFB = cumulative fluid balance, CVP = central venous pressure

Click here to view


The patient was intubated in the resuscitation room and given mechanical ventilation with an initial SIMV mode of 15/14/7/100%. Initial blood gas analysis (BGA): pH/pCO2/pO2/BE/SaO2: 7,268/59.4/190/27,2/0/99. During treatment in the ICU, the patient received positive pressure ventilation to support oxygenation, a GCS score of 6, crackles in both lung fields, an increase in CVP of 14 mmHg, and creatinine of 0.7 mg/dL. The patient was given furosemide at 5 mg/h to reduce and remove excess fluid.

After 24 h of treatment in the ICU, the patient showed improvement. The crackles in both lung fields began to decrease from before, the CVP began to decrease to 11 mmHg and obtained a urine output of 1.5 mL/kg BW/h, sCr of 1.9 mg/dL, and the CFB was −250. On the fifth day, the creatinine examination was repeated, and the sCr value was 0.4 mg/dL. The patient was fully conscious, and the CVP was decreasing by 1–3 mmHg; urine output was 0.8 mL/kg BW/h, with a negative CFB of −1170.


  Discussion Top


In this case of drowning, the patient experiences a passive entry of fluid into the respiratory tract, resulting in excess fluid in the lungs, which causes the patient to experience hypoxia. Prolonged hypoxia causes a neurological disorder. Obvious neurological disturbances are one of the symptoms that arise due to hypoxia-induced brain edema.[4] The administration of PEEP and diuretics, as well as the fluid management in the ICU, plays a role in improving pulmonary oxygenation.

The usual treatment for brain edema is the administration of diuresis, either mannitol or furosemide. The use of diuretics in the management of drowning cases is aimed at eliminating fluid intake and reducing organ congestion. The administration of furosemide has two effects, namely on the renal and vascular. The direct vascular effect of diuretics triggers vasodilation, an increase in venous compliance that causes a decrease in venous pressure and capillary hydrostatic pressure resulting in transcapillary refill. Furthermore, there will be an increase in plasma protein concentration and colloid osmotic pressure. The mechanism that occurs in the diffusion of fluid into the intravascular compartment is due to hydrostatic pressure and an increase in colloid osmotic pressure, both of which increase the colloid hydrostatic gradient.[5]

In this case, after the administration of furosemide, the body volume status was reduced, indicated by a decrease in the CVP value of about 5–6 mmHg and a good urinary response to diuretics. After the discontinuation of furosemide, a large urine output of about 3.6 cc/kg/h was maintained with a CVP monitoring of 1–3 mmHg. Furosemide in reducing interstitial edema helps lymphatic function in the flow phase. Diuresis, which was characterized by a very negative cumulative balance in this case, which was −2.5 L in 48 h, was proven to be safe for the kidneys as indicated by normal creatinine. The installation of a central venous catheter is intended as an access to vasopressors and to see the status of body fluids. At the initial measurement, the CVP was 10 mmHg, and fluid removal with furosemide drip was performed to treat pulmonary edema that occurred with a lower CVP target. Based on Guyton’s concept, a decrease in venous return can be caused by a high CVP value so that the gradient between the mean circulatory filling pressure and right atrial pressure decreases.[6] Reduced venous return causes congestion in the organs. In studies of increased ICU mortality, the incidence of acute kidney injury (AKI) was associated with positive cumulative balance and high CVP scores.[5],[7]

Based on the case series, CVP can be used as a guide for resuscitation in septic patients with fluid overload and AKI. Resuscitation was carried out either pharmacologically (furosemide) or mechanically in the case series with a CVP target of 0–2 mmHg. From this case series report, we found improvement in systemic oxygenation, improvement in AKI without hemodynamic instability, and a negative cumulative balance associated with a decrease in vasopressor dose.[8] Decreased CVP values due to reduced body fluid status can also reduce brain structure and improve venous return and cerebral drainage. This is in accordance with the improvement in the patient’s neurological status, namely, an improvement in consciousness to compos mentis, and the patient was successfully extubated.[9]


  Conclusion Top


Furosemide causes fluid moves into the intravascular and is then excreted through the urine through the effect of natriuresis in the kidneys. Furosemide is given when the CVP is more than 5 mmHg and is discontinued when the CVP is less than 5 mmHg. In this case, after the administration of furosemide, the body volume status was reduced, indicated by a decrease in the CVP value of about 5–6 mmHg and a good urinary response to diuretics. After the discontinuation of furosemide, a large urine output of about 3.6 cc/kg/h was maintained with a CVP monitoring of 1–3 mmHg. Furosemide in reducing interstitial edema helps lymphatic function in the flow phase. Diuresis that was characterized by a very negative cumulative balance of −2500 cc in 48 h was proven to be safe for the kidneys as indicated by normal values of creatinine.

Acknowledgment

Not applicable.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Authors contributions

EYL has made substantial contributions to the conception; design of the work; literature search; acquisition; clinical studies; experimental studies; and interpretation of data. YG and AS have made contributions to the concept; design of work; data analysis; statistical analysis; article review; and guarantor. AD has contributed to article preparation and article editing.

Consent to participate

The authors certify that they have obtained all appropriate consent forms. The patient will understand that names and initials will not be published, and due efforts will be made to conceal the identity.

Ethical approval

Not applicable.



 
  References Top

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Mott TF, Latimer KM. Prevention and treatment of drowning. Am Fam Physician 2016;93:576-82.  Back to cited text no. 1
    
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Ogbu OC, Murphy DJ, Martin GS. How to avoid fluid overload. Curr Opin Crit Care 2015;21:315-21.  Back to cited text no. 2
    
3.
Legrand M, Soussi S, Depret F. Cardiac output and CVP monitoring… to guide fluid removal. Crit Care 2018;22:89.  Back to cited text no. 3
    
4.
Caricato A, Conti G, Della Corte F, Mancino A, Santilli F, Sandroni C, et al. Effects of PEEP on the intracranial system of patients with head injury and subarachnoid hemorrhage: The role of respiratory system compliance. J Trauma 2005;58:571-6.  Back to cited text no. 4
    
5.
Dewi NL, George YWH. Case report: Central venous pressure-guided de-resuscitation in sepsis patients with fluid overload induced acute kidney injury. Crit Care Shock 2017;20:109-14.  Back to cited text no. 5
    
6.
Prabhakar H, Sandhu K, Bhagat H, Durga P, Chawla R. Current concepts of optimal cerebral perfusion pressure in traumatic brain injury. J Anaesthesiol Clin Pharmacol 2014;30:318-27.  Back to cited text no. 6
[PUBMED]  [Full text]  
7.
Hasanin AM, Amin SM, Agiza NA, Elsayed MK, Refaat S, Hussein HA, et al. Norepinephrine infusion for preventing postspinal anesthesia hypotension during cesarean delivery: A randomized dose-finding trial. Anesthesiology 2019;130:55-62.  Back to cited text no. 7
    
8.
Vincent JL, Taccone FS, He X. Harmful effects of hyperoxia in postcardiac arrest, sepsis, traumatic brain injury, or stroke: The importance of individualized oxygen therapy in critically ill patients. Can Respir J 2017;2017:2834956.  Back to cited text no. 8
    
9.
Dubowitz DJ, Dyer EA, Theilmann RJ, Buxton RB, Hopkins SR. Early brain swelling in acute hypoxia. J Appl Physiol (1985) 2009;107:244-52.  Back to cited text no. 9
    


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