Volume Kinetic (VK) Shock or Volumetric Overload Shocks (VOS) In Surgical Patients

Ghanem AN

Published on: 2020-12-03

Abstract

“Volume kinetic (VK) shocks are cardiovascular shocks induced by acute substantial volume changes of the cardiovascular system in either direction by decrease or increase”. A decrease in cardiovascular volume induces the long established and well-known hypovolemic and hemorrhagic shocks. Cardiovascular shocks induced by volumetric overload (VO) have been recently reported. Volume kinetic (VK) shocks or Volumetric Overload Shocks (VOS) are common iatrogenic complication of fluid therapy in hospitals that is overlooked and underestimated. It may present in theatre as cardiopulmonary arrest or later with coma and acute respiratory distress syndrome (ARDS). VOS is 2 types: VOS1 and VOS2. VOS1 is induced by 3.5-5 liters of sodium-free fluid and is characterized with dilution HN that has 2 nadirs and 2 paradoxes, is most dynamic and illusive and currently has a lifesaving therapy of 5%NaCl or 8.4%NaCo3. VOS2 may complicate VOS1 or occur de novo complicating sodium-based fluid therapy during resuscitation of shock, acutely ill patients, and prolonged surgery. It has no obvious serological markers or none. Between 3-10 liters of sodium-based fluids induce VOS 2, and 12-14 liters cause mortality. Many errors and misconceptions mislead physicians into giving too much fluid for resuscitation due to faulty rules on fluid therapy dictated by the wrong Starling's law. The correct replacement for this law is the hydrodynamic of the porous orifice (G) tube. These scientific discoveries should make the Medical World wake up and pay attention.

Keywords

Shock; Volume kinetic shock; Hyponatraemia; Fluid therapy; The TURP syndrome; ARDS; Starling's law; Capillary-ISF transfer

Introduction

Cardiovascular system in either direction by decrease or increase. A decrease in cardiovascular volume induces the long established and well-known hypovolemic and hemorrhagic shocks. Cardiovascular shocks induced by volumetric overload (VO) have been recently reported [1-4]. Volumetric overload shocks (VOS) are iatrogenic complications of fluid therapy in hospitals [1-3]. It is overlooked and underestimated. When it is realized that acute dilution hyponatraemia (HN) and the acute respiratory distress syndrome (ARDS) is representative of each type of VOS it would be appreciated that it has staggering morbidity, cost, and mortality. It affects hundreds of thousands of patients worldwide each year including surgical, urological, and obstetric patients of men, women and children undergoing surgery. It concerns new discoveries in physics, physiology, and medicine [4]. The objective of this article is to bring these new discoveries into the attention of readers, particularly Anesthetists and Surgeons as these conditions concerns them most.

The scientific discoveries include 2 VOS [1-3], proving the physiological law of Starling wrong and finding a new correct replacement which is the hydrodynamic of the porous orifice (G) tube (Figure 1) [5-7]. Starling's law being wrong has resulted in many errors and misconceptions on fluid therapy [8] during prolonged surgery and the resuscitation of shock and the acutely ill patients. This misleads physicians into giving too much fluid which induces VOS, causing cardiac or respiratory arrest or both "cardiopulmonary arrest" immediately in theatre [9] or the acute respiratory distress syndrome (ARDS) later [10,11].

Figure 1 shows a diagrammatic representation of the hydrodynamic of G tube based on G tubes and chamber C. This 37-years old diagrammatic representation of the hydrodynamic of G tube in chamber C is based on several photographs. The G tube is the plastic tube with narrow inlet and pores in its wall built on a scale to capillary ultra-structure of precapillary sphincter and wide inter cellular cleft pores, and the chamber C around it is another bigger plastic tube to form the G-C apparatus. The chamber C represents the ISF space. The diagram represents a capillary-ISF unit that should replace Starling’s law in every future physiology, medical and surgical textbooks, and added to chapters on hydrodynamics in physics textbooks. The numbers should read as follows:

  1. The inflow pressure pushes fluid through the orifice
  2. Creating fluid jet in the lumen of the G tube**.
  3. The fluid jet creates negative side pressure gradient causing suction maximal over the proximal part of the G tube near the inlet that sucks fluid into lumen.
  4. The side pressure gradient turns positive pushing fluid out of lumen over the distal part maximally near the outlet.
  5. Thus, the fluid around G tube inside C moves in magnetic field-like circulation (5) taking an opposite direction to lumen flow of G tube.
  6. The inflow pressure 1 and orifice 2 induce the negative side pressure creating the dynamic G-C circulation phenomenon that is rapid, autonomous, and efficient in moving fluid and particles out from the G tube lumen at 4, irrigating C at 5, then sucking it back again at 3,
  7. Maintaining net negative energy pressure inside chamber C.

**Note the shape of the fluid jet inside the G tube (Cone shaped), having a diameter of the inlet on right hand side and the diameter of the exit at left hand side (G tube diameter). I lost the photo on which the fluid jet was drawn, using tea leaves of fine and coarse sizes that runs in the centre of G tube leaving the outer zone near the wall of G tube clear. This may explain the finding in real capillary of the protein-free (and erythrocyte-free) sub-endothelial zone in the Glycocalyx paradigm (Woodcock and Woodcock 2012) [3]. It was also noted that fine tea leaves exit the distal pores in small amount maintaining a higher concentration in the circulatory system than that in the C chamber- akin to plasma proteins.

VOS are two types depending on the type of fluid inducing it: VOS1 is induced by sodium-free fluid such as 5% Glucose and/or 1.5% Glycine used as irrigating fluid during the transurethral resection of the prostate (TURP) surgery. It is known in urology as the TURP syndrome [12] or hyponatraemic shock [13].

This VOS1 is induced by 1.5% Glycine absorption and 5% glucose infusion of about 3.5-5 liters or >5% of body weight and is characterized with dilution hyponatraemia (HN) [13,14]. It has 2 nadirs and 2 paradoxes [15-18] making it dynamic and illusive [16-18]. The 2 nadirs are: The immediate drop of serum sodium level as result of dilution of the extra-cellular fluid that occurs during or immediately after surgery. The second nadir is that occurring later within 24 hours after water shift into the intracellular compartment causing spontaneous elevation of serum sodium level towards normal, yet the clinical picture gets worse due to generalized cellular edema. This cellular edema manifests as the multiple organ dysfunction syndromes (MODS). The 2 paradoxes are: A pathological volumetric overload induces hypotensive shock of VOS and acute kidney injury (AKI) which is paradoxical to the response of physiological volume replacement that treats hypotensive shock and induces diuresis [14].

VOS 1 currently has a lifesaving therapy of hypertonic sodium therapy (HST) of 5% NaCl or 8.4% NaCo3 [19]. It may present with cardiopulmonary arrest [9] or one or more of the other manifestations of MODS- being the new name for ARDS [10,11]. The clinical manifestations include in addition to cardiorespiratory features: coma, AKI, and hepatic dysfunction. It also causes coagulopathies and excessive bleeding at the surgical site (Table 1). VOS 1 affects women too during the trans-cervical resection of endometrium due to 1.5% Glycine absorption, or during Cesarean section due to excessive 5% Glucose infusion [13,14].

Table 1: the manifestations of VOS 1 of the TURP syndrome for comparison with ARDS manifestations induced by VOS2.


Cerebral

Cardiovascular

Respiratory

Renal

Hepatic & GIT

Numbness

Tingling

SBB1

COC2

Convulsions

Coma

PMBCI 3

Hypotension

Bradycardia

Dysrhythmia

CV Shock*

Cardiac Arrest

Sudden Death

 

Cyanosis.

FAM4

APO)5

RA6

Arrest

CPA7

Shock lung

ARDS$

Oliguria

Annuria8

Renal failure or

AKI9

Urea ↑

Creatinine ↑

 

Dysfunction:

Bilirubin ↑

SGOT ↑

Alkaline Phosphatase ↑.

GIT symptoms.

DGR10

       Paralytic ileus

Nausea & Vomiting.

Table Abbreviations

SBB1 Sudden bilateral blindness

COC2 Clouding of consciousness

PMBCI3 Paralysis mimicking bizarre cerebral infarctions, but is recoverable on instant use of HST of 5%NaCl and/or NaCo3, and so is coma and AKI

FAM4 Frothing around the mouth

APO5 Acute pulmonary oedema

RA6 Respiratory arrest

CPA7 Cardiopulmonary arrest

ARDS $ Manifests later on ICU

AKI9 Acute kidney injury

DGR10 Delayed gut recovery

CV Shock* Cardiovascular shock of VOS reported here as VOS 1 and VOS2.

Annuria8 That is unresponsive to diuretics but responds to HST of 5%Ncl and/or 8.4%NaCo3

AKI8 Acute kidney injury

Also occurs the excessive bleeding at the surgical site and

Leukocytosis occurred in the absence of sepsis and septic shock

VOS is always mistaken for one of the recognized shocks such as hemorrhagic and septic shocks hence wrongly treated with further volume expansion using sodium-based isotonic fluids. This induces VOS2 and cardiopulmonary arrest that has no serum markers of HN [2] and causes ARDS in patients who survive a little longer [8,9]. Multiple regression analysis has proved that volumetric overload is the most significant factor in causing the clinical picture of VOS (Figures 2,3 and Table 2).

Figure 2 shows the means and standard deviations of volumetric overload in 10 symptomatic patients presenting with shock and hyponatraemia among 100 consecutive patients during a prospective study on transurethral resection of the prostate. The fluids were of Glycine absorbed (Gly abs), intravenously infused 5% Dextrose (IVI Dext) Total IVI fluids, Total Sodium-free fluid gained (Na Free Gain) and total fluid gain in liters.

Figure 3 shows volumetric overload (VO) quantity (in litres and as percent of body weight) and types of fluids. Group 1 was the 3 patients who died in the case series as they were misdiagnosed as one of the previously known shocks and treated with further volume expansion. Group 2 were 10 patients from the series who were correctly diagnosed as volumetric overload shock and treated with hypertonic sodium therapy (HST). Group 3 were 10 patients who were seen in the prospective study and subdivided into 2 groups; Group 3.1 of 5 patients treated with HST and Group 3.2 of 5 patients who were treated with guarded volume expansion using isotonic saline.

P

T Value

Std. Value

Std. Err

Value

Parameter

 

 

0.773

 

 

Intercept

0.0001

3.721

1.044

0.228

0.847

Fluid Gain (l)

0.0212

2.42

-0.375

00.014

0.033

Osmolality

0.0597

1.95

0.616

0.049

0.095

Na+ (C_B)

0.4809

0.713

0.239

0.087

0.062

Alb (C_B)

0.2587

1.149

-0.368

0.246

-0.282

Hb (C_B)

0.4112

0.832

-0.242

5.975E-5

-4.973E-5

Glycine (C_B)

Table 2 shows the multiple regression analysis of total per-operative fluid gain, drop in measured serum osmolality (OsmM), sodium, albumin, Hb and increase in serum glycine occurring immediately post-operatively in relation to signs of the TURP syndrome. Volumetric gain and hypo-osmolality are the only significant factors. The significance of volumetric overload is remarkable.

Volumetric overload shock type 2 (VOS 2) [1-3,10] is induced by massive infusion of sodium-based fluids such as normal saline, Hartmann, plasma, plasma substitutes and blood. VOS 2 may complicate VOS1 or is induced by sodium-based fluid during fluid therapy for resuscitation of shock and the critically ill and prolonged surgery and presents with ARDS later. Volumetric gain of 12-14 liters of sodium-based fluids reported in the first article on ARDS [20] which is the only article in the whole literature, other than the articles of mine some of which are referenced here, that documents the volume of retained fluid in ARDS- until very recently.

The Recent Supporting Evidence on VOS and ARDS

Professor Hahn studied VK in healthy volunteers and patients [21,22]. He reported in conclusion that: "Guidelines for fluid therapy rarely take into account that adverse effects occur in a dose-dependent fashion. Adverse effects of crystalloid fluids are related to their preferential distribution to the interstitial of the subcutis, the gut, and the lungs. The gastrointestinal recovery time is prolonged by 2 days when more than 2 liters is administered. Infusion of 6-7 liters during open abdominal surgery results in poor wound healing, pulmonary oedema, and pneumonia. There is also a risk of fatal postoperative pulmonary oedema that might develop several days after the surgery. Even larger amounts cause organ dysfunction by breaking up the interstitial matrix and allowing the formation of lacunae of fluid in the skin and central organs, such as the heart. For both crystalloid and colloid fluids, coagulation becomes impaired when the induced hemodilution has reached 40%. Coagulopathy is aggravated by co-existing hypothermia. Although oedema can occur from both crystalloid and colloid fluids, these differ in pathophysiology."

Other authors also found a significant effect of crystalloids overload on mortality as they did the research during the first 24-48 hours from hospital admission. I have found only one study on adults' trauma patients by Jones et al (2016) [23], and one paediatrics study by Coons et al (2018) [24] and a remarkable review article by Schrier reported in 2010 [25] that incriminate saline overload and recommend judicious use of fluid infusion during resuscitation. In patients of these adult and paediatric trauma trials there is no sepsis involved and both were done over a period of 24 and 48 hours, respectively. Both articles detected a significant relationship of VO with morbidity and mortality of ARDS.

Jones et al [23] reported: "Large-volume crystalloid resuscitation is associated with increased mortality and longer time ventilated. Based on this data, we recommend judicious use of crystalloids in the resuscitation of trauma patients.”

The conclusion by Coons et al [24] was: "Early administration of high volumes of crystalloid fluid greater than 60 ml/kg/day significantly correlates with pulmonary complications, days NPO, and hospital length of stay. These results span the first 48 h of a patient's hospital stay and should encourage surgical care providers to exercise judicious use of crystalloid fluid administration in the trauma bay, ICU, and floor"

The huge prospective multicenter trials [27,28] also documented massive volumetric overload (VO) in surviving ARDS patients of 3-10 liters of retained fluid volume but have neither recognized VOS nor incriminated VO in the patho-aetiology of ARDS. They also did not recognize the high association of VO with the mortality which was estimated at 60 or 90 days not at the immediate period of 24-48 hours after admission as demonstrated by the above reports [23,24]. Excellent example of these huge multicenter trials is that study reported by Rowan et al in 2017 [26}.

In the results section, Rowan et al reported: “Each study day the liberal-strategy group received more fluid than the conservative-strategy group and on days 1 through 4 had a lower urinary output, resulting in a higher cumulative fluid balance (Table 2). During the study, the seven-day cumulative fluid balance was -136±491 ml in the conservative-strategy group, as compared with 6992±502 ml in the liberal-strategy group (P<0.001) (Figure 1 of the Supplementary Material). For patients who were in shock at baseline, the cumulative seven-day fluid balance was 2904±1008 ml in the conservative-strategy group and 10,138±922 ml in the liberal-strategy group (P<0.001). For patients who were not in shock at baseline, the cumulative fluid balance was −1576±519 ml in the conservative-strategy group and 5287±576 ml in the liberal-strategy group (P<0.001)”

Therapy of VOS and ARDS

Prevention

Being iatrogenic complications of fluid therapy, both VOS and ARDS are preventable.

To prevent VOS and ARDS a limit to the maximum amount of fluid used during shock resuscitation or major surgery must be agreed upon (New guidelines are required).

Surgical care providers must exercise judicious use of crystalloid fluid administration in the trauma bay, ICU, and floor.

Replace the loss in haemorrhagic hypovolemic shocks but do not overdo it.

If hypotension develops despite volume replacement later during ICU stay, inotropic drugs, hydrocortisone 200 mg and hypertonic sodium therapy (HST) should be used-please, see later. The latter restores the pre-capillary sphincter tone (peripheral resistance) so that the capillary works as normal G tube again, but NO isotonic crystalloids or colloids over-infusions is required.

To learn the new correct science, one must unlearn the old incorrect habits.

The following practices should be abandoned:

  • Bolus fluid therapy in surgical patients
  • Abandon the aggressive current liberal regimen of Early Goal-Directed Therapy (EGDT) in treating shocked and septic patients [26]. Multiple huge multicenter trials have proved it to be the wrong practice.
  • Please refrain from persisting to elevate CVP to levels above 12 and up to 18-22 cm saline in shock management. This is a major cause for inducing VOS and ARDS during shock resuscitation, particularly septic shock.

Therapeutic

Hypertonic sodium therapy (HST) of 5%NaCl and/or 8.4%NaCo3 has truly proved lifesaving therapy for the TURP syndrome and acute dilution HN as well as secondary VOS 2 that complicates fluid therapy of VOS 1 causing ARDS. It works by inducing massive diuresis being a potent suppressor of antidiuretic hormone. It may also work on the pre-sphincter capillary restoring its tone.

My experience in using it for treating established ARDS with sepsis and primary VOS 2 that causes ARDS is not tested. However, evidence on HST suggests it will prove successful if given early, promptly and adequately to ARDS patients while refraining from any further isotonic crystalloid or colloid fluid infusions using saline, HES and/or plasma therapy- just give the normal daily fluid requirement and no more. After giving HST over one hour using the CVP catheter already inserted, the patient recovers from AKI and produces through a urinary catheter massive amount of urine of 4-5 liters as you watch. This urine output should not be replaced. Just observe the patient recovering from his AKI, coma and ARDS and asks for a drink. This is done in addition to the cardiovascular, respiratory, and renal support on ICU. Patients with AKI on dialysis, the treating nephrologist should aim at and set the machine for inducing negative fluid balance.

The HST of 5%NaCl and/or 8.4%NaCo3 is given in 200 ml doses over 10 minutes and repeated. I did not have to use more than 1000 ml during the successful treatment of 16 ARDS patients. Any other hypertonic sodium concentration is not recommended. A dose of intravenous diuretic may be given but it does not work in a double or triple the normal dose. A dose of 200 mg of hydrocortisone is most useful. Antibiotic prophylactic therapy is given in appropriate and adequate doses to prevent sepsis and septic shock. No further fluid infusions of any kind crystalloids, colloids and blood is given. The urinary loss should not be replaced as this defeats the objective of treatment.

A Suggested Recommended Future Trial

I would recommend a small pilot prospective controlled cohort study on 100 patients as a start to try HST in established ARDS cases that would be something to look forward to reading a report on it, hopefully soon. No multicenter trial or high expenses is needed for that. Not much time is required either. If you cannot do it on a hundred patients, you probably cannot (as Mr JP Ward put it to me before the start of our prospective study12). I can assure the investigators that no harm will come to patients. It is a guaranteed win bit; you may win but you do not lose anything. In the worst-case scenario, the patient may not respond because of chronicity of ARDS or after sepsis complicates ARDS and gets the capillary damage established. As the author of all self-referenced articles here, published in open access journals, and as copyright holder I give open permission to any interested investigator to use any of my articles as template, particularly recommended article [12] - the appropriate permission from the editors of BJUI and authors are given. I strongly recommend that hypertonic sodium therapy should be given a trial in the management of both sepsis and Covid-19 as it may prove to be my successful positive contribution to the war against the Covid-19 pandemic.

Conclusion

Volume kinetic shocks or VOS are common iatrogenic complication of fluid therapy in hospitals that is overlooked and underestimated. It may present in theatre as cardiopulmonary arrest or later with coma and ARDS. VOS is 2 types: VOS1 and VOS2. VOS1 is induced by3.5-5 liters of sodium-free fluid and is characterized with dilution HN that has 2 nadirs and 2 paradoxes, is most dynamic and illusive and currently has a lifesaving therapy of 5%NaCl and/or 8.4%NaCo3. VOS2 may complicate VOS1 or occur de novo complicating sodium-based fluid therapy during resuscitation of shock, acutely ill patients and prolonged surgery. It has no obvious serological markers or none. It is induced by 3-10 liters of sodium-based fluids and 12-14 liters characterize the dead ARDS patients, Many errors and misconceptions mislead physicians into giving too much fluid for resuscitation due to faulty rules on fluid therapy dictated by the wrong Starling's law. The correct replacement for this law is the hydrodynamic of the porous orifice (G) tube.

References

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