key: cord-0005899-k4vloxx1
authors: Allen, P. W.; Thornton, M.; Gordon, M. W. G.; Robertson, C. E.; Dawes, J.; Hughes, K. R.; Armstrong, R. F.; Coolen, L.; Dens, J.; Baeck, E.; Claes, C.; Lins, R. L.; Verbraeken, H.; Daelemans, R.; Gilbert, J.; Smith, B.; Davenport, A.; Aulton, K.; Payne, R. B.; Will, E. J.; Guerin, C.; Pozzetto, B.; Berthoux, F.
title: Correspondence
date: 1989
journal: Intensive Care Med
DOI: 10.1007/bf00273572
sha: 68b698e30d23d88337ad5eff8f2797713b6fd961
doc_id: 5899
cord_uid: k4vloxx1

nan

In their report of oesophageal perforation with minitracheostomy (Intensive Care Medicine 1989; 15:140-141), Drs. Claffey and Phelan state that despite adherance to the manufacturer's guidelines the tube passed lateral to the trachea to perforate the oesophagus in two patients.

Three simple modifications to technique make this loss of midline orientation less likely. First, stand at the head of the bed not at the side. Second, while infiltrating with local anaesthetic, pass the needle through the cricothryroid membrane aspirating air to identify the trachea and spray local anaesthetic onto the mucosa to reduce coughing and venous bleeding on incision. Finally, when the short, guarded scalpel blade is correctly inserted through the cricothyroid membrane it will usually stand there with a little support from an assistant. The left hand remains splinting the tissues on each side of the blade while the other hand picks up and aligns the introducer. The blade is then lifted clear by the assistant allowing immediate, easy insertion of the introducer.

The use of a Seldinger technique for cricothyrotomy may well prove easier and safer, however, the suggestion to modify the "Minitrach" technique to an open method using a longer blade seems to defeat the object of the procedure and takes us back to the florid description by Chevalier Jackson in 1921 [1] .

Yours faithfully, P.W. Allen and M. Thornton 

Neutrophils have been demonstrated to accumulate in the lung parenchyma in the Adult Respiratory Distresss Synchrome (ARDS) where they are capable of releasing proteolytic enzymes, eicosanoids and free oxygen radicals. Neutrophil elastase (HNE) is a constituent of the primary (azurophil) granules of the human neutrophil and is released as the result of neutrophil activation [1] . In addition to degrading elastin, this protease enzyme acts against a wide range of other substrates including fibrinogen, complement components, fibronectin, plasminogen and immunoglobulins. It is currently believed to be important in the genesis of inflammatory tissue injury. Measurement of released neutrophil elastase provides a sensitive indicator of neutrophil activation. The aim of this study was to investigate whether neutrophil elastase plasma levels were elevated during the trauma process, together with the time course and levels involved.

Eleven patients were studied, 9 males and 2 females, with an age range 19-80 years (mean 43 years). All had sustained injuries as a result of a road traffic accident or a fall from a height. All patients were admitted directly from the scene of the accident to the resuscitation room of the Accident and Emergency Department at the Royal Infirmary of Edinburgh.

Venous blood samples were taken on the patients' admission to the resuscitation room, with the exception of one patient whose first sample was taken the following morning. Six patients had at least one further sample taken during the course of their hospital admission. The blood was centrifuged immediately, the plasma removed and stored at -20 °C. The concentrations of neutrophil elastase in the samples were subsequently measured using a radio-immunoassay technique for human neutrophil elastase similar to that of Plow [2] . The antibody used was produced in-house using rabbit polyclonal antisera. The antigen used was purified from human neutrophils after leucopboresis and was pure by gel electrophoresis. (The antigen was supplied courtesy of Dr. R Davies, Merck, Sharp and Dome Ltd). The antibody has absolute specificity for neutrophil elastase and does not cross-react with pancreatic or platelet elastases. It detects HNE equally well as the free enzyme or when HNE is complexed with its inhibitors. The coefficient of variation within and between assays was less than 5%.

In the 10 patients who had samples taken within a few minutes of arrival, the initial level was significantly elevated. The range was 34-299ng/ml, mean 125.5_+82.3ng/ml with 99.9% confidence limits 39.9-21/.2ng/ml (Fig. 1) . The normal range was 18.7_+ 10.1 ng/ml with 99.9% confidence limits of 15.1-22.3 ng/ml and n = 80 (Fig. 1 ). Levels fell progressively in those patients who were studied serially.

In order to determine whether there was any relationship between the severity of injury and the maximum concentration of human neutrophil elastase, Injury Severity Scores (ISS) were calculated for each patient using the Abbreviated Injury Scale [3] . The range of scores was 10-75. However, there was no direct correlation between the ISS and the peak level of neutrophil elastase (r = -0.1928; p = 0.57).

This study demonstrates that traumatised patients have very high levels of human neutrophil elastase detectable within minutes of sustaining their injury. The rapidity of rise in HNE leads to speculation about the mechanism whereby neutrophils are activated during the trauma process.

Previous work on patients with burn injury has indicated that maximal levels of neutrophil activation occur during the first 5 days after injury, while complement activation peaks on post-burn days 6 to 8 or later [4] . This provides strong evidence to support the theory that initial neutrophil activation in injured patients is mediated by mechanisms other than the complement pathway -be it the classic or the alternative one. Davis et al. felt that endotoxin was the most likely candidate and have demonstrated that endotoxin activates neutrophils at concentrations much lower than those required to activate complement [4] . Furthermore, endotoxin is known to be detectable in the circulation shortly after injury [5] .

The absence of direct correlation between the severity of injury and HNE plasma levels is difficult to explain. There is a number of possible aetiologies. The lack of correlation between HNE and ISS may reflect an exogenous stimulus being involved. The neutrophil elastase level may reflect the total mass of injured tissue rather than the clinical severity of a particular injury [6] . Or a more general response to trauma that involves not only the size of the injury but HNE nglml 300. Further studies are underway to delineate the mechanisms involved in early neutrophil activation following trauma. Meanwhile, further investigation is required into the relationship between neutrophil elastase and the development of ARDS and other local tissue complications following trauma. 

Dear Sir, Acute hypercalcaemia carries a significant mortality [1, 2] . Therapeutic interventions include intravenous fluids (saline), diuresis, steroids, diphosphonates, mithramycin, intravenous phosphate and acute haemodialysis or haemofiltration. Occasionally, despite these measures, the plasma calcium does not fall. We report a case which suggests that urgent surgical exploration of the neck may be indicated in this situation.

A 34-year-old negro male was admitted with a 5 day history of anorexia and weakness, abdominal pain, weight loss and vomiting. On examination, he was pyrexial 38 °C, tachycardic (100/min) and tachypnoeic (30/min). He had epigastric tenderness and a mass on the right side of his neck.

Investigations showed: sodium 132 mmol/1, potassium 2.4 mmol/1, urea 26.7 mmol/1, creatinine 36 umol/1, bicarbonate 29mmol/1, chloride 90mmol/l, calcium 5.2mmol/1, albumin 44 g/l, corrected calcium 4.9 mmol/1, phosphate 1.58 mmol/1, haemoglobin 152 g/l, white blood count 18 x 109 and positive sickle cell trait. Hand, skull X-rays, CXR, and ECG were normal. A differential diagnosis of primary hyperparathyroidism or myeloma was made. Treatment was started with rehydration, potassium replacement, and steroids. The bone marrow result was non-diagnostic.

The patient deteriorated rapidly in the 6 h after admission, becoming unrousable and his respiratory rate increased to 40/min. Artrial blood gases (FiO 2 = 0.4) were pH 7.3, PaO 2 6.5 kPa and PaCO 2 4.5 kPa. Central venous pressure and pulmonary capillary wedge pressure measurements were normal (3-9cms H20 and 10-14 mmHg). His CXR showed diffuse patchy shadowing.

He was intubated and ventilated, but his condition continued to deteriorate (PaO 2 7.0 kPa, PaCO 2 7.0 kPa, pH 7.22) [(FiO 2 = 0.6), minute volume of 12 1 and 5 cm PEEP]. Despite rehydration, frusemide, hydrocortisone, calcitonin and mithramycin his calcium rose to 5.7 mmol/L. Examination of the neck revealed a mass which was confirmed on ultrasound. The patient proceeded to emergency exploration of the neck hut profound hypotension, resistant to massive inotropic support resulted in the patient's death after removal of a 35 g parathyroid adenoma.

In a patient with severe refractory hypercalcaemia, therapeutic measures may be unsucessful. If therapy fails, a parathyroid adenoma should be considered as a possible diagnosis. Early surgical exploration of the neck will not compromise the prognosis if the hypercalcaemia is associated with a malignancy, but may well save the patient's life if the diagnosis is hypercalcaemic crisis. 

Dear Sir,

We wish to report the case of a 43-year-old slaughterhouse worker with meningitis, permanent perceptive deafness and bilateral endophthalmitis due to Streptococcus suis type II (group R). This is only the third case of Str. suis infection occurring in our cot~ntry [1] and to our knowledge only the second case with serious endophthalmitis which has been reported in the literature [2] .

The patient was admitted with a two days history of fever, diarrhea and vomiting. He was lethargic but responsive to questioning. Blood pressure was 120-80 mm Hg, pulse rate 100/min and temperature 37.9 °C. Neurologic examination revealed marked nuchal rigidity, symmetric tendon reflexes, plantar reflexes were flexor and the pupils were reactive but slightly unequal. Ocular movements, speech and hearing were normal. No papilledema was seen. Blood examination showed a leucocytosis of 13x109/1 and a thrombocytopenia of 52 × 109/1. Lumbar puncture yielded turbid cerebrospinal fluid (CSF) containing 2160WBC/mm 3 (80% neutrophils) and Gram positive cocci (Table 1) . Treatment was started with benzylpenicillin 24 million units/day. By the second day there was progressive hearing and visual loss. On audiovestibular examination a total perceptive hearing loss and spontaneous right sided nystagmus were noted. Cold caloric testing with ice-water gave no vestibular reaction in either ear. Ophthalmological examination showed the absence of light perception due to bilateral endophthalmitis. Severe bilateral anterior uveitis and posterior synechiae were found on slit lamp examination. The intraocular pressure was normal. The pres- (Table 1) . Several months later there was still a total perceptive bearing loss in both ears and total vestibular areflexia. There was only light perception in the left eye. Str. suis type II is a well recognised cause of septicaemia, meningitis and purulent arthritis in young pigs [3] . Since 1968 more than 70 cases of human infection, mostly after exposure to pig meat, have been reported [3] . In gram-stained smears and even after culture Str. suis frequently is mistaken for a pneumococcus or enterococcus [3, 4] . Damage to the eighth cranial nerve with vertigo and varying degrees of hearing loss are well known [3, 5] . Endophthalmitis has only been reported in one previous case where Str. suis strains were grown from an anterior chamber tap [2] . Because complications of this infection are very severe and bacteriological identification is not always easy, physicians should suspect Str. suis infection in any patient with meningitis who works in the pig meat industry. Yours sincerely, 

In their interesting paper regarding the efficacy of high frequency jet ventilation (HFJV) in dogs with oleic-acid induced pulmonary edema [1] Hachenberg et al. conclude that "both in interstitial and alveolar-edema continuous positive pressure ventilation (CPP¥) is more effective than HFJV" and extend their animal model observations to the clinical setting. Since our laboratory and clinical findings in similar pathophysiological states do not completely coincide with their findings, we would like suggest that because of legitimate but overstated concerns about "auto-PEEP" the authors may have used a less than optimal setting for HFJV, thus prejudicing their results.

The authors compare HFJV utilizing a frequency of 3 Hz and a driving pressure of 1.5 bar, without PEEP, with CPPV utilizing a PEEP of 0.5 kPa. The resultant mean airway pressure was significantly higher in the CPPV mode than for HFJV. The work of Fusciardi et al. [2] and the three other authors quoted by Hachenberg et al. supports the concept that mean airway pressure is a major determinant of gas exchange and oxygenation in diseased lungs. It would appear that HFJ¥, as utilized in this experiment, was inferior to CPPV. To justify this difference in mean airway pressures the authors refer to four papers showing that HFJV produces hidden "auto-PEEP" which they say may account for more than 0.6 kPa [3] [4] [5] [6] .

In reviewing these papers we find that Simon [3] and Saari [4] both used a high frequency oscillator and not a jet ventilator. In addition, both authors used frequencies which were for the most part much higher than were utilized in this experiment. Eliasen [5] used a jet ventilator and specifically stated that no "auto-PEEP" was found at frequencies less than 5 Hz. Rouby [6] found that HFJV induced a "PEEP effect" but considered that it was only significant in patients with normal or increased lung compliance and specifically recommended the jet ventilator for "all types of respiratory failure characterized by decreased lung volumes, low pulmonary compliance, or chest wall rigidity", a description that would fit the model utilized by Hachenberg et al. It would therefore appear that none of these papers supports the assumptions about "auto-PEEP" in this model. It is possible that use of HFJV with lower frequency, higher drive pressure and the application of PEEP would have resulted in the authors coming to a different conclusion about the relative value of HFJV and CPPV in the acutely injured lung.

Dear Sir,

The currently commercially available replacement fluids for haemofiltration are acetate or lactate based. Lactate is converted to bicarbonate on an equimolar basis via the Cori cycle. Indeed treatment using large volumes of lactate based fluids in continuous high volume haemofiltration/and or dialysis in patients with adequate hepatic function can result in a metabolic alkalosis [1] . If the rate of administration of lactate exceeds the rate of metabolism, hyperlactataemia occurs. However-previous reports have suggested that hyperlactataemia has no adverse consequences [2, 3] . We report a case in which sequential haemofiltration treatments resulted in increasing hyperlactataemia and acidosis.

A 24-year-old man developed fulminant hepatic failure and oliguric renal failure following paracetamol (acetaminophen) self poisoning. On admission he was in grade 4 hepatic coma and required ventilation. Serum urea 13.4 mmol/1 (81 mg/dl), creatinine 787~mol/1 (8.9mg/dl), alanine transferase 6.071iu/1 (normal < 15 iu/1), alkaline phosphatase 12.1 KAu/dl (normal < 13), bilirubin 132 gmol/1 (normal < 15), and prothrombin ratio 8.6 (normal <1.1). Despite volume expansion and dopamine (5 gg/kg/min), he remained oliguric, urine volume less than 5 ml/h. He was therefore treated by daily machine haemofiltration using a polyamide haemofilter (Gambro FH77, Gambro AB, Lurid, Sweden), blood pump speed 200 ml/min, transmembrane pressure 200 mmHg, and minimal heparinisation was required. A typical isovolaemic 17 1 exchange of fluid was completed in 3.5-3.9 h using a lactate based fluid (Filtrasol 22, containing 45 mmol/1) of a racaemic mixture of D and L lactate).

Arterial blood lactate was measured during each treatment, samples were collected into buffered cetrimide (ICI, Macclesfield, UK) and sodium fluoride, and analysed using an Analox LM2 (Analox, Hammersmith, UK). In addition the arterial hydrogen ion concentration ([H+]) and serum bicarbonate were also measured.

Prior to each treatment, circulating volume was corrected if necessary, and an isovolaemic exchange was undertaken. Mean arterial blood pressure remained in excess of 80 mmHg during all five treatments.

There was a serial increase in the degree of hyperlactataemia during the five haemofiltration treatments (Fig. 1) . During the first two treatments the [H +] decreased and serum bicarbonate increased as expected. Thereafter, [H+I increased progressively, from 35 to 50 nmol/1 (normal range 35 -45 nmol/1) during the fifth treatment, and serum bicarbonate fell progressively, from 23.5 mmol/1 to ARTERIAL LACTATE rnrnol/l 10- One explanation for the paradoxical increases in [H +] would be that as liver function was severely affected, the rate of conversion of lactate to bicarbonate was less than the rate at which bicarbonate was lost to the ultrafiltrate, and therefore the acidosis was due to bicarbonate loss. However, the absolute bicarbonate loss in the ultrafiltrate was consecutively less with each treatment, being 513 mmol for the first and 342 mmol for the fifth. Thus bicarbonate loss cannot be the explanation. Hyperlactataemia results in the intracelhilar accumulation of lactate, and in vitro this has been shown to reduce the cytosolic phosphorylation potential and so reduce the amount of ATP available for energy dependent metabolism and cell function [4] . In vivo lactate accumulation has been shown to affect cardiac function by reducing ventricular muscle contraction [5] . It may be that in patients with severe liver failure, who have disturbances of tissue oxygen delivery that hyperlactatemia by affecting cellular energy dependent mechanisms causes a vicious circle to develop, and that bicarbonate based fluids are required in the management of these special cases.

Yours sincerely, A. Davenport, K. Aulton, R.B. Payne and E.J. Will

Dear Sir, Benign histiocytic proliferation with marked hemophagocytosis demonstrated by bone marrow histology has been reported in association with active viral infection and has been named virus associated hemophagocytic syndrome (VAHS) [3] . We report a case of VAHS which was possibly related to Coxsackie virus A 9 infection in a non-immunosuppressed adult who had a systemic illness with comatose encephalitis, acute renal failure and hepatitis.

Case history. A 56-year-old woman, with no past medical history, was admitted to our ICU (DO) from a general hospital where she had been referred with fever (38.7°C), chills, sweating, diarrhoea, generalized macular rash and diffuse arthritis. On admission, the patient was somnolent and mildly icteric, without fever. Physical examination revealed a left ptosis, liver enlargement, petechial put-pura on the legs and hands but no splenomegaly nor lymphadenopathy. Liver cytolysis (SGOT 480 IU/L, SGPT 232/L), non-oliguric acute renal failure (serum creatinine 541pmol/1) and profound hyponatremia (plasma sodium 112 retool/l) were noted. The prothrombin time was 67°70 and the fibrinogen level was 1.6 g/1. 31 h later, she developed seizures, despite a normalized plasma sodium, and required intubation, mechanical ventilation and IV barbiturate therapy. Her CSF was clear and contained 3 mrnol/1 glucose, 0.68g/1 protein and 40 lymphocytes/ml. Cerebral computed tomography was normal. Simultaneously blood leukopenia and thrombopenia developed (WBC count: 4200/ml, 66°70 neutrophils at DO and 1800/ml, 29°7o neutrophils at D2; platelet count 25 000/ml at DO and 10000/ml at D2). Bone marrow smears demonstrated proliferation of large histiocytes with erythocyte and neutrophil hemophagocytosis, no abnormal cells were seen. From DI3, the bone marrow aplasia reversed with a significant reduction of histiocytic proliferation and renal function improved, as did liver function. The conscious level improved slowly allowing spontaneous ventilation via a tracheotomy tube. The seizures persisted and continued IV therapy was required. Septic shock associated with a venous catheter led to death 5 months later. Cultures of blood, urine, respiratory secretions, CSF and stools (which were also inoculated into suckling mice) were negative for bacteria, parasites and viruses. Cerebral and hepatic biopsy tissue showed non-specific inflammatory lesions and were sterile on culture. Serological tests for a broad spectrum of agents showed no evidence for infection with the exception of neutralizing antibodies against coxsackie A9 (Fig. 1) . Serology was also negative for other enteroviruses (echoviruses 7, 8, 11; coxsaekie B 4 and B 5). A part from the serum neopterin and the neopterin/creatinine ratio being 10 times the normal value (Fig. 1) , the rest of the immunological workup was normal.

Discussion. Apart from the absence of lymphadenopathy this case closely resembles other reported cases of VAHS [3, 5] . In contrast to the 14 immunosuppressed patients reported in [3] , our patient was immunocompetent. Viruses previously implicated in this syndrome are cytomegalovirus, Epstein-Barr virus, varicella-zoster virus and adenoviruses [3, 5] . In another report an enterovirus (coxsackie B 5) infection was suspected in a 12-year-old girl at the onset of Still's disease [2] .

The case we have reported is to our knowledge only the second reported case of VAHS related to an enterovirus infection, demonstrated by serological evidence. The high levels of neopterin production related to acute viral infection in renal transplantation [1, 4] , is an additional, although non-specific, indication of viral infection in our patient. As the production of neopterin by macrophages is induced by gamma interferon released from activated T lympho-cytes, we speculate that this activation of macrophages contributed to the histiocytic proliferation.

Yours sincerely, C. Guerin, B. Pozzetto and F. Berthoux

High-frequency jet ventilation during oleic-acid induced pulmonary edema

Hemodynamic consequences of increasing mean airway pressure during high frequency jet ventilation

Mean airway pressure and alveolar pressure during high-frequency ventilation

Lung inflation durign high frequency ventilation

Peripheral airway pressure during high frequency ventilation

Factors influencing pulmonary volumes and CO 2 elimination during high frequency ventilation

Hypochloraemic alkalosis after high flux continuous haemofiltration and continuous arteriovenous haemofiltration with dialysis

Lactate haemodialysis

Lactic acidosis: diagnosis and treatment

Cytosolic phosphoarylation potential

Mechanisms of reduction of action potential duration of ventricular myocardium by exogenous lactate

Monitoring of the serum neopterin/creatinine ratio in renal transplantation

Still's disease associated with coxsackie infection and hemophagocytic syndrome

Virus-associated hemophagocytic syndrome. A benign histiocytic proliferation distinct from malignant histiocytosis

Assessment of plasma neopterin in clinical kidney transplantation

Epstein-Barr virus-associated hemophagocytic syndrome: virological and immunopathological studies

Service de N6phrologie